A Heart Risk Factor Even Doctors Know Little About
To millions of Americans, Bob Harper was the picture of health, a celebrity fitness trainer who whipped people into shape each week on the hit TV show “The Biggest Loser.”
But last February, Mr. Harper, 52, suffered a massive heart attack at a New York City gym and went into cardiac arrest. He was saved by a bystander who administered CPR and a team of paramedics who rushed him to a hospital, where he spent two days in a coma.
When he awoke, Mr. Harper was baffled, as were his doctors. His annual medical checkups had indicated he was in excellent health. How could this have happened to someone seemingly so healthy?
The culprit, in turned out, was a fatty particle in the blood called lipoprotein(a). While doctors routinely test for other lipoproteins like HDL and LDL cholesterol, few test for lipoprotein(a), also known as lp(a), high levels of which triple the risk of having a heart attack or stroke at an early age.
For most people, lp(a) is nothing to worry about. Levels are strongly determined by genetics and the majority of people produce very little of it.
But up to one in five Americans, including Mr. Harper, have perilously high levels of it in their blood. Studies show that diet and exercise have almost no impact on lp(a), and cholesterol-lowering drugs only modestly lower it.
“People don’t know about it, physicians don’t know about it, and we have to get an education program out there, but that’s expensive,” said Dr. Henry N. Ginsberg, the Irving Professor of Medicine at Columbia University and a leading expert on lp(a). “I would say that somewhere between 15 to 20 percent of the population would clearly benefit from knowing that this is their problem.”
Lp(a) was discovered in 1963 by a Norwegian scientist, Kare Berg, who noticed that it was especially common among people with coronary heart disease. No one knows precisely what purpose lp(a) serves in the body, though some scientists speculate that it may have a beneficial role such as helping to repair injured cells or preventing infections by binding to pathogens in the blood.
But the downside of excessive lp(a) is clear: It accelerates the formation of plaque in the arteries, and it promotes blood clots.
“It’s sort of a double whammy,” said Dr. Donald Lloyd-Jones, a cardiologist at the Northwestern University Feinberg School of Medicine who helped write the American Heart Association’s cholesterol guidelines. “Biologically, lp(a) both gets into the artery wall and causes damage there more easily.”
Studies suggest that the threshold for high lp(a) begins around 30 milligrams per deciliter of blood. Heart disease risk jumps for those in the 80th percentile, with lp(a) levels above 60, and climbs sharply for the 5 percent of the population with lp(a) levels between 150 and 300, according to Dr. Ginsberg at Columbia. “Those people can be disasters in terms of cardiovascular risk,” he said.
Yet many people at high risk do not fit the typical profile of a person with heart disease. Sandra Revill Tremulis was a health-conscious medical device executive who moonlighted as an aerobics instructor, followed a strict diet, and maintained 16 percent body fat, equivalent to that of an elite athlete. Her LDL and total cholesterol levels were low, and at age 39, her Framingham risk score, which gauges heart disease risk, put her odds of having a heart attack in her 40s at just 1 percent.
But when she started experiencing extreme fatigue and struggled to finish her workouts, she went to an interventional cardiologist and asked for a thorough work-up — which revealed that she had a 95 percent blockage in one of her coronary arteries.
“I was imminent to have a widow-maker heart attack at age 39,” she said.
Further testing showed she had high lp(a), which she believes she inherited from her father, who died of a heart attack at age 50. Determined to raise awareness, Ms. Revill Tremulis started a nonprofit, the Lipoprotein(a) Foundation, and now travels the globe advocating for wider testing.
“Only a small percentage of physicians know about this,” she said. “The biggest challenge for patients is finding knowledgeable physicians who know about this and can help them.”
Dr. Lloyd-Jones at Northwestern said that testing for lp(a) should be considered for people with early-onset cardiovascular disease — which means younger than age 50 for men and age 60 for women — or a strong family history of it. Since high lp(a) is hereditary, those who have it often have a parent, sibling or grandparent who suffered a premature heart attack or stroke. When one person has it, it’s important to test other family members too.
“It’s what we call cascade screening, looking for affected first-degree relatives,” Dr. Lloyd-Jones said.
Once high lp(a) is identified, doctors try to mitigate its effects by controlling other risk factors. They aggressively lower patients’ LDL cholesterol, optimize their blood pressure and blood sugar, and strongly encourage healthy diet and exercise habits.
Two medications, niacin and a class of drugs known as PCSK9 inhibitors, have been shown to modestly reduce lp(a) levels. But niacin, a B vitamin, has many side effects, and PCSK9 inhibitors, which are not approved for lp(a) lowering, are not usually covered by insurance for that purpose and can cost as much as $14,000 a year.
At least one drug company, Akcea Therapeutics, a spinoff of Ionis Pharmaceuticals, is developing a drug specifically to combat lp(a), but the drug is still in mid-stage testing and it could be years before it reaches the market.
Since his heart attack, Mr. Harper of “The Biggest Loser” has embarked on a newfound mission to raise awareness about heart disease and to urge people to get tested for lp(a).
His days no longer revolve around intense and grueling workouts, he said. Instead he believes the key to being healthy is managing stress, getting proper sleep, eating a balanced diet and enjoying life because it could end at any moment, an approach he has outlined in his new book, “The Super Carb Diet.”
“Being healthy is not about what you can do in the gym,” Mr. Harper said. “It’s not about what you can do on the outside. It’s what’s going on in the inside. I really needed to find out what was going on with me, and that’s what this did. It woke me up.”
2016年12月25日星期日
Statins CAN cause heart disease - Shock research warns drug risks hardened arteries
CONTROVERSIAL drug statins can actually increase the risk of heart disease, shock new research has shown.
People taking the drugs are more likely to suffer from hardening of the arteries, a leading cause of heart problems.
In addition, researchers found the drugs block a process that protects the heart.
This can “cause, or worsen, heart failure”, according to a study.
The lead author says: “I cannot find any evidence to support people taking statins.”
The findings, published in Expert Review of Clinical Pharmacology, will add to the debate surrounding the drugs, which are routinely given to up to 12 million patients in the UK, or around one in four adults.
Supporters say they save lives by lowering cholesterol and UK health regulators say they are safe.
Oxford professor Sir Rory Collins has warned that overstating concerns about statins could “cause very large numbers of unnecessary deaths from heart attacks and stroke”.
Opponents have pointed to the side effects, such as skeletal weakness and muscle pain, and say the risks outweigh the benefits.
Now Professor Harumi Okuyama, whose team studied a series of more than 20 major research papers on the drugs, says they could cause heart disease.
Dr Okuyama, of Nagoya City University, Japan, said: “We have collected a wealth of information on cholesterol and statins from many published papers and find overwhelming evidence that these drugs accelerate hardening of the arteries and can cause, or worsen, heart failure. I cannot find any evidence to support people taking statins and patients who are on them should stop.”
The researchers say the hypothesis that statins protect the heart by lowering cholesterol is flawed and that high cholesterol is not necessarily linked to heart disease.
They also found statins have a negative effect on vital body processes linked to heart health.
They discovered patients taking the drugs were more likely to have calcium deposits in their arteries, a phenomenon directly linked to heart attacks.
This is because statins block a molecule needed for the body to produce a vital K vitamin, which prevents calcification of the arteries.
Dr Okuyama and his team say many earlier industry-sponsored studies, which show the benefits of statins, are unreliable.
They claim this is because they were carried out before new European regulations were introduced in 2004 which insisted on all trial findings, both negative and positive, being declared.
The study states that before these new rules came into effect “unfair and unethical problems were associated with clinical trials reported by industry-supported scientists”.
Dr Okuyama’s team looked at studies before and after 2004.
They found: “The epidemic of heart failure and atherosclerosis (hardening of the arteries) that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically re-evaluated.”
Dr Malcolm Kendrick, who has studied heart health and statins, said: “This study demolishes the argument that these drugs should be prescribed to anyone, as the harms clearly outweigh any previously suggested benefits.”
Dr Peter Langsjoen, a heart specialist based in Texas who is co-author of the study, said: “Statins are being used so aggressively and in such large numbers of people that the adverse effects are now becoming obvious. These drugs should never have been approved for use. The long-term effects are devastating.”
A spokesman for the MHRA, the Government drug regulator, said: “The benefits of statins are well established and are considered to outweigh the risk of side effects in the majority of patients. "Any new significant information on the efficacy of statins will be carefully reviewed and action be taken if required"
People taking the drugs are more likely to suffer from hardening of the arteries, a leading cause of heart problems.
In addition, researchers found the drugs block a process that protects the heart.
This can “cause, or worsen, heart failure”, according to a study.
The lead author says: “I cannot find any evidence to support people taking statins.”
The findings, published in Expert Review of Clinical Pharmacology, will add to the debate surrounding the drugs, which are routinely given to up to 12 million patients in the UK, or around one in four adults.
Supporters say they save lives by lowering cholesterol and UK health regulators say they are safe.
Oxford professor Sir Rory Collins has warned that overstating concerns about statins could “cause very large numbers of unnecessary deaths from heart attacks and stroke”.
Opponents have pointed to the side effects, such as skeletal weakness and muscle pain, and say the risks outweigh the benefits.
Now Professor Harumi Okuyama, whose team studied a series of more than 20 major research papers on the drugs, says they could cause heart disease.
Dr Okuyama, of Nagoya City University, Japan, said: “We have collected a wealth of information on cholesterol and statins from many published papers and find overwhelming evidence that these drugs accelerate hardening of the arteries and can cause, or worsen, heart failure. I cannot find any evidence to support people taking statins and patients who are on them should stop.”
The researchers say the hypothesis that statins protect the heart by lowering cholesterol is flawed and that high cholesterol is not necessarily linked to heart disease.
They also found statins have a negative effect on vital body processes linked to heart health.
They discovered patients taking the drugs were more likely to have calcium deposits in their arteries, a phenomenon directly linked to heart attacks.
This is because statins block a molecule needed for the body to produce a vital K vitamin, which prevents calcification of the arteries.
Dr Okuyama and his team say many earlier industry-sponsored studies, which show the benefits of statins, are unreliable.
They claim this is because they were carried out before new European regulations were introduced in 2004 which insisted on all trial findings, both negative and positive, being declared.
The study states that before these new rules came into effect “unfair and unethical problems were associated with clinical trials reported by industry-supported scientists”.
Dr Okuyama’s team looked at studies before and after 2004.
They found: “The epidemic of heart failure and atherosclerosis (hardening of the arteries) that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically re-evaluated.”
Dr Malcolm Kendrick, who has studied heart health and statins, said: “This study demolishes the argument that these drugs should be prescribed to anyone, as the harms clearly outweigh any previously suggested benefits.”
Dr Peter Langsjoen, a heart specialist based in Texas who is co-author of the study, said: “Statins are being used so aggressively and in such large numbers of people that the adverse effects are now becoming obvious. These drugs should never have been approved for use. The long-term effects are devastating.”
A spokesman for the MHRA, the Government drug regulator, said: “The benefits of statins are well established and are considered to outweigh the risk of side effects in the majority of patients. "Any new significant information on the efficacy of statins will be carefully reviewed and action be taken if required"
2016年11月3日星期四
Flax Seeds Can Have Profound Effect on Hypertension
A recent article in the journal, Meat Science, acknowledged that a sector of the population perceives meat as a food that is detrimental to their health because of studies associating meat consumption with heart disease and cancer. So, the article continues, meat consumers may look for healthier food alternatives as a means to maintain good health, which represents a good opportunity for the meat industry to develop some new products. The industry felt that natural foods could be added to meat to reach those health-oriented consumers by boosting antioxidants levels, for example. Foods like flax seeds and tomatoes are healthy, associated with reduced risks of cancer and cardiovascular disease. So by making flax-y tomato burgers, they figure they can reduce saturated fat intake and maybe eat less sugar somehow. Wouldn’t it be easier to just cut out the middle-cow and eat flax seeds ourselves?
Flax seeds have been described as a “miraculous defense against some critical maladies.” I’m a fan of flax, but this title seemed a bit over-exuberant; I figured something just got lost in translation, but then I found a prospective, double-blinded, placebo-controlled, randomized trial—you know how hard that is in a nutrition study? For drugs, it’s easy: you have two identical looking pills, one’s active, one’s placebo, and until the end of the study, neither the researcher nor the patient has any idea which is which, hence “double blind.” But people tend to notice what they’re eating. So how did they sneak a quarter cup of ground flax seeds into half of the people’s diets without them knowing? They created all these various flax or placebo containing foods, and even added bran and molasses to match the color and texture, so it was all a big secret until six months later when they broke the code to see who ate which.
Why test it on hypertension? Because having a systolic blood pressure over 115—that’s the top number—may be the single most important determinant for death in the world today. If you take a bunch of older folks, most of them on an array of blood pressure pills, and don’t improve their diet at all, despite the drugs, they may start out on average hypertensive and stay hypertensive six months later. But those who were unknowingly eating ground flaxseeds every day, dropped their systolic blood pressure about ten points, and their diastolic, the lower number, by about seven points. That might not sound like a lot, but a drop like that could cut stroke risk 46 percent and heart disease 29 percent, and that ten point drop in the top number could have a similar effect on strokes and heart attacks. And for those that started out over 140, they got a 15-point drop.
In summary, flaxseed induced one of the most potent antihypertensive effects ever achieved by a dietary intervention. In other words, the magnitude of this decrease in blood pressure demonstrated by dietary flaxseed, is as good or better than other nutritional interventions and comparable to many drugs, which can have serious side effects. And they’re not exaggerating about the comparable to drugs bit. The flax dropped systolic and diastolic up to 15 and 7. Compare that to powerful ACE inhibitors like Vasotec, which may only drop pressures five and two, and calcium channel blockers like Norvasc or Cardizem which drop pressures eight and three. Side effects of these drugs include a large list of serious medical issues, as seen in my video Flax Seeds for Hypertension, compared to the side effect of flax seeds, “its pleasant nutty flavor.”
During the six-month trial there were strokes and heart attacks in both groups, though. Even if the flax seeds can cut risk in half, any avoidable risk is unacceptable. Isn’t high blood pressure just inevitable as we get older? No – the prevalence of hypertension does increase dramatically with age, but not for everyone. People who eat more plant-based diets or keep their salt intake low enough tend not to exhibit any change in blood pressure with advancing age. It’s always better to prevent the disease in the first place.
2016年10月19日星期三
Extreme Nutrition: The Diet of Eskimos
The carnivorous diet of traditional Eskimo inhabitants of the frozen, northern, circumpolar regions of planet Earth (Siberia, Alaska, Canada, and Greenland), serves as a testament to the strengths and adaptability of the human species. The foods consumed by these hardy people are in "polar" opposition to those recommended by me (the McDougall Diet of starches, vegetables, and fruits): a carnivore vs. an herbivore diet. Unfortunately, misinformation surrounding the all-meat diet of the Eskimo has promoted dangerous eating habits to the modern-day general public.
For more than 6,000 years, natives of the frozen North have lived with almost no contact with the rest of the world. Not until the mid-1800s were reliable records made of their daily lives, their diets, and their health. Early reports describe these people as looking beautiful and athletic when they were young, but then they aged quickly, and "men and women who appeared to be 60 or over were rare."
Rumors have since circulated that traditional Eskimos have lived free of heart disease, cancer, and most other chronic diseases affecting western civilizations these days. Research published in the mid-1970s tried to explain this "Eskimo paradox" of living healthy with very few plant foods, on a high-fat, high-cholesterol, no-dietary-fiber diet. The omega-3 fish fats were noted as the miracle ingredient providing protection. Dietetic and medical experts have uncritically accepted this theory in the face of libraries filled with incriminating evidence to the contrary. They tell patients to eat more fish, poultry, and even red meat—like the Eskimos – and plenty of fish oil - in order to stay healthy.
Pushing the Nutritional Envelope
Hunted animals, including birds, caribou, seals, walrus, polar bears, whales, and fish provided all the nutrition for the Eskimos for at least 10 months of the year. And in the summer season people gathered a few plant foods such as berries, grasses, tubers, roots, stems, and seaweeds. Frozen snow-covered lands were unfit for the cultivation of plants. Animal flesh was, by necessity, the only food available most of the time.
The fat, not the protein, from animal foods provided most of the 3,100 calories required daily for these active people. Plants are the primary source of all carbohydrates, including digestible sugars and non-digestible dietary fibers. Eating raw meat indirectly provided Eskimos with enough carbohydrates in the form of glycogen (found in the muscles and liver of animals) to meet their necessary nutrient requirements and keep them out of a starvation condition called ketosis. Muscle tissue contains almost no calcium, and as a result the daily intake was about 120 mg/day versus the 800 mg and more commonly recommended for good health. Plants (not people) synthesize Vitamin C, yet the Eskimo was able to avoid scurvy with the 30 mg of vitamin C consumed daily found in land and sea animals. Recommendations for vitamin C are 60 mg/day and higher daily. Low levels of sunlight, and preformed vitamin D from fish, met the "sunshine D vitamin" requirement for Eskimo health. By the grace of environmental design, Nature made sure there was just enough nutrition for the Eskimo to survive.
There Is No Eskimo Paradox
The human being is designed to thrive on a diet of starches, vegetables and fruits. The Eskimo experience serves as a testament to the miraculous strengths and adaptability of our bodies. We can survive on raw and cooked meat, but we thrive on starches, vegetables and fruits. These hardy people survived living at the edge of the nutritional envelope, but not in good health. Here are some of the health costs they paid:
Eskimos Suffer from Atherosclerosis
Claims that Eskimos were free of heart (artery) disease are untrue. A thorough review of the evidence concludes that "Eskimos have a similar prevalence of CAD (coronary artery disease) as non-Eskimo populations, they have excessive mortality due to cerebrovascular strokes, their overall mortality is twice as high as that of non-Eskimo populations, and their life expectancy is approximately 10 years shorter than the Danish population."
Mummified remains of Eskimos dating back 2,000 years have shown extensive hardening of the arteries throughout their brains, hearts and limbs; as a direct consequence of following a carnivorous diet of birds, caribou, seals, walrus, polar bears, whales, and fish. The June 1987 issue of National Geographic magazine carried an article about two Eskimo women, one in her twenties and the other in her forties, frozen for five centuries in a tomb of ice. When discovered and medically examined they both showed signs of severe osteoporosis and also suffered extensive atherosclerosis, "probably the result of a heavy diet of whale and seal blubber."
Eskimos Suffer from Severe Bone Loss
Their low-calcium diet and lack of sunshine (vitamin D) are only minor factors contributing to the extensive osteoporosis found in recent and ancient Eskimos. Alaskan Eskimos older than age 40 have been found to have a 10% to 15% greater deficit in bone mineral density compared to Caucasians in the US. This research published in 1974 on 107 elderly people concluded, "Aging bone loss, which occurs in many populations, has an earlier onset and greater intensity in the Eskimos. Nutritional factors of high protein, high nitrogen, high phosphorus, and low calcium intakes maybe implicated."
Protein, and especially animal protein, consumed in excess of our needs places serious burdens on the body. The liver and kidneys work hard to process the excess protein and excrete its byproducts along with the urine. As a result of this extra work, Eskimos have been reported to have an enlarged liver while living on meat, and to produce larger than average volumes of urine in order to excrete the byproducts of protein metabolism. The bones also play a role in managing excess animal protein (acidic by nature) by neutralizing large amounts of dietary acids. In this process bone structure and bone mineral content are lost through the kidney system, depleting the bones into a condition called osteoporosis.
Eskimos Are Infected with Parasites
Diseases of animals are readily transmitted to humans when eaten. One example is trichinosis (an infection with the roundworm Trichinella spiralis), which is found in about 12% of older Eskimos; a result of eating raw and infected walrus, seal, and polar bear meat. In most cases this parasite infestation causes no symptoms, but illness and death can result.
Meat-derived Chemical Pollution
Since the 1970s the diet of the Eskimo has contained high levels of toxic, organic pollutants and heavy metals. These lipophilic chemicals are attracted to and concentrated in the fatty-tissues of land and sea animals. As a direct result of the traditional Eskimo diet (now contaminated by industry wastes), the bodies of these Arctic people contain the highest human concentrations of environmental chemicals found anywhere on Earth: "levels so extreme that the breast milk and tissues of some Greenlanders could be classified as hazardous waste." Eskimo women have been found to have levels of PCBs in their breast milk five to ten times higher than women in southern Canada. These chemicals cause and promote many forms of cancer and cause brain diseases, including Parkinson's disease.
Nutrition Has Gone Downhill for the Eskimo
The notion that consuming meat, fish, and fish oil will promote health and healing has captured the attention of the scientific community in large part because of the misinterpretation** of the Eskimo experience. But life has gotten worse for the Eskimo. Over the past 50 years their traditional diet has been further modified with the addition of western foods. Rather than using a hook, spear, or club to catch their meal, as in the past, people living in this part of the world use the "green lure" (the dollar bill) and catch their meals through an open car window at the local fast-food restaurant. Obesity, type-2 diabetes, tooth decay, and cancers of the breast, prostate, and colon have been added to the Eskimo's traditional health problems of artery disease, bone loss, and infectious diseases.
People living in the frozen north these days have heated homes and drive around in comfortable SUVs. The challenging environment their ancestors barely survived through required a carnivorous diet. Those days of needing 3100 calories a day to counter the freezing cold and hunt for dinner are gone. The idea that current epidemics of obesity and sickness in these Northern people would be best fixed by returning to the old ways of carnivorous diet would not work unless they also returned to living in igloo homes and hunted their lands for every meal. Physicians and dietitians now caring for these people suffering from the western diet with the addition of too much traditional food (ancestral meat) should be prescribing a starch-based diet to help them lose excess weight and cure common dietary diseases.
*The term "Eskimo" comes from a Native American word that may have meant "eater of raw meat." The word "Eskimo" has come to be considered offensive, especially in Canada. Many prefer the name "Inuit," which means "the people" or "real people." However, "Eskimo" is the term used in the scientific and historical literature and will be used here.
**Misinterpretation is easy to spread because:
1) People love to hear good news about their bad habits.
2) Nutritional "facts," even when false and harmful, are used to sell meat, fish, and other foods.
3) The media loves headlines that sell their products, like "The Eskimo Diet proves Meat's Good."
For more than 6,000 years, natives of the frozen North have lived with almost no contact with the rest of the world. Not until the mid-1800s were reliable records made of their daily lives, their diets, and their health. Early reports describe these people as looking beautiful and athletic when they were young, but then they aged quickly, and "men and women who appeared to be 60 or over were rare."
Rumors have since circulated that traditional Eskimos have lived free of heart disease, cancer, and most other chronic diseases affecting western civilizations these days. Research published in the mid-1970s tried to explain this "Eskimo paradox" of living healthy with very few plant foods, on a high-fat, high-cholesterol, no-dietary-fiber diet. The omega-3 fish fats were noted as the miracle ingredient providing protection. Dietetic and medical experts have uncritically accepted this theory in the face of libraries filled with incriminating evidence to the contrary. They tell patients to eat more fish, poultry, and even red meat—like the Eskimos – and plenty of fish oil - in order to stay healthy.
Pushing the Nutritional Envelope
Hunted animals, including birds, caribou, seals, walrus, polar bears, whales, and fish provided all the nutrition for the Eskimos for at least 10 months of the year. And in the summer season people gathered a few plant foods such as berries, grasses, tubers, roots, stems, and seaweeds. Frozen snow-covered lands were unfit for the cultivation of plants. Animal flesh was, by necessity, the only food available most of the time.
The fat, not the protein, from animal foods provided most of the 3,100 calories required daily for these active people. Plants are the primary source of all carbohydrates, including digestible sugars and non-digestible dietary fibers. Eating raw meat indirectly provided Eskimos with enough carbohydrates in the form of glycogen (found in the muscles and liver of animals) to meet their necessary nutrient requirements and keep them out of a starvation condition called ketosis. Muscle tissue contains almost no calcium, and as a result the daily intake was about 120 mg/day versus the 800 mg and more commonly recommended for good health. Plants (not people) synthesize Vitamin C, yet the Eskimo was able to avoid scurvy with the 30 mg of vitamin C consumed daily found in land and sea animals. Recommendations for vitamin C are 60 mg/day and higher daily. Low levels of sunlight, and preformed vitamin D from fish, met the "sunshine D vitamin" requirement for Eskimo health. By the grace of environmental design, Nature made sure there was just enough nutrition for the Eskimo to survive.
There Is No Eskimo Paradox
The human being is designed to thrive on a diet of starches, vegetables and fruits. The Eskimo experience serves as a testament to the miraculous strengths and adaptability of our bodies. We can survive on raw and cooked meat, but we thrive on starches, vegetables and fruits. These hardy people survived living at the edge of the nutritional envelope, but not in good health. Here are some of the health costs they paid:
Eskimos Suffer from Atherosclerosis
Claims that Eskimos were free of heart (artery) disease are untrue. A thorough review of the evidence concludes that "Eskimos have a similar prevalence of CAD (coronary artery disease) as non-Eskimo populations, they have excessive mortality due to cerebrovascular strokes, their overall mortality is twice as high as that of non-Eskimo populations, and their life expectancy is approximately 10 years shorter than the Danish population."
Mummified remains of Eskimos dating back 2,000 years have shown extensive hardening of the arteries throughout their brains, hearts and limbs; as a direct consequence of following a carnivorous diet of birds, caribou, seals, walrus, polar bears, whales, and fish. The June 1987 issue of National Geographic magazine carried an article about two Eskimo women, one in her twenties and the other in her forties, frozen for five centuries in a tomb of ice. When discovered and medically examined they both showed signs of severe osteoporosis and also suffered extensive atherosclerosis, "probably the result of a heavy diet of whale and seal blubber."
Eskimos Suffer from Severe Bone Loss
Their low-calcium diet and lack of sunshine (vitamin D) are only minor factors contributing to the extensive osteoporosis found in recent and ancient Eskimos. Alaskan Eskimos older than age 40 have been found to have a 10% to 15% greater deficit in bone mineral density compared to Caucasians in the US. This research published in 1974 on 107 elderly people concluded, "Aging bone loss, which occurs in many populations, has an earlier onset and greater intensity in the Eskimos. Nutritional factors of high protein, high nitrogen, high phosphorus, and low calcium intakes maybe implicated."
Protein, and especially animal protein, consumed in excess of our needs places serious burdens on the body. The liver and kidneys work hard to process the excess protein and excrete its byproducts along with the urine. As a result of this extra work, Eskimos have been reported to have an enlarged liver while living on meat, and to produce larger than average volumes of urine in order to excrete the byproducts of protein metabolism. The bones also play a role in managing excess animal protein (acidic by nature) by neutralizing large amounts of dietary acids. In this process bone structure and bone mineral content are lost through the kidney system, depleting the bones into a condition called osteoporosis.
Eskimos Are Infected with Parasites
Diseases of animals are readily transmitted to humans when eaten. One example is trichinosis (an infection with the roundworm Trichinella spiralis), which is found in about 12% of older Eskimos; a result of eating raw and infected walrus, seal, and polar bear meat. In most cases this parasite infestation causes no symptoms, but illness and death can result.
Meat-derived Chemical Pollution
Since the 1970s the diet of the Eskimo has contained high levels of toxic, organic pollutants and heavy metals. These lipophilic chemicals are attracted to and concentrated in the fatty-tissues of land and sea animals. As a direct result of the traditional Eskimo diet (now contaminated by industry wastes), the bodies of these Arctic people contain the highest human concentrations of environmental chemicals found anywhere on Earth: "levels so extreme that the breast milk and tissues of some Greenlanders could be classified as hazardous waste." Eskimo women have been found to have levels of PCBs in their breast milk five to ten times higher than women in southern Canada. These chemicals cause and promote many forms of cancer and cause brain diseases, including Parkinson's disease.
Nutrition Has Gone Downhill for the Eskimo
The notion that consuming meat, fish, and fish oil will promote health and healing has captured the attention of the scientific community in large part because of the misinterpretation** of the Eskimo experience. But life has gotten worse for the Eskimo. Over the past 50 years their traditional diet has been further modified with the addition of western foods. Rather than using a hook, spear, or club to catch their meal, as in the past, people living in this part of the world use the "green lure" (the dollar bill) and catch their meals through an open car window at the local fast-food restaurant. Obesity, type-2 diabetes, tooth decay, and cancers of the breast, prostate, and colon have been added to the Eskimo's traditional health problems of artery disease, bone loss, and infectious diseases.
People living in the frozen north these days have heated homes and drive around in comfortable SUVs. The challenging environment their ancestors barely survived through required a carnivorous diet. Those days of needing 3100 calories a day to counter the freezing cold and hunt for dinner are gone. The idea that current epidemics of obesity and sickness in these Northern people would be best fixed by returning to the old ways of carnivorous diet would not work unless they also returned to living in igloo homes and hunted their lands for every meal. Physicians and dietitians now caring for these people suffering from the western diet with the addition of too much traditional food (ancestral meat) should be prescribing a starch-based diet to help them lose excess weight and cure common dietary diseases.
*The term "Eskimo" comes from a Native American word that may have meant "eater of raw meat." The word "Eskimo" has come to be considered offensive, especially in Canada. Many prefer the name "Inuit," which means "the people" or "real people." However, "Eskimo" is the term used in the scientific and historical literature and will be used here.
**Misinterpretation is easy to spread because:
1) People love to hear good news about their bad habits.
2) Nutritional "facts," even when false and harmful, are used to sell meat, fish, and other foods.
3) The media loves headlines that sell their products, like "The Eskimo Diet proves Meat's Good."
2016年9月4日星期日
LOW-CALORIE DIET FOR TYPE 2 DIABETES
In 2013, we awarded our largest ever research grant of £2.4 million to understand the impact of a low calorie diet on Type 2 diabetes.
Professor Roy Taylor at Newcastle University and Professor Mike Lean at the University of Glasgow are comparing the long-term effects of a new weight management approach to the best diabetes care currently available.
The aim is to find out if an intensive weight management plan can help people put their Type 2 diabetes into remission for the long term.
The DiRECT study
What is the background to this research?
Not everyone with Type 2 diabetes is overweight, but weight gain and obesity are the most important risk factors for Type 2 diabetes and the reason why Type 2 has become a global epidemic that affects overweight people of all ages.
Surgical operations, such as gastric banding and gastric bypass, are potential solutions because they lead to dramatic weight loss, which can put Type 2 diabetes into remission for up to 80% of patients. But these treatments are expensive, invasive and carry a risk of surgical complications, which mean they can only be offered as a last resort.
What do we know already about low-calorie diets?
In 2011, a Diabetes UK research trial at Newcastle University tested a low-calorie diet in 11 people with Type 2 diabetes, which helped us to understand how Type 2 diabetes can be put into remission.
After the 8-week diet, volunteers had reduced the amount of fat in their liver and pancreas. This helped to restore their insulin production and put their Type 2 diabetes into remission. Three months later, some had put weight back on, but most still had normal blood glucose control.
This study was only a first step. It was designed to tell us about the underlying biology of Type 2 diabetes, and it followed the participants for only three months.
Another study, published in 2016, confirmed these findings and showed (in 30 people) that Type 2 diabetes could be kept in remission 6 months after the low-calorie diet was completed. It also suggested that the diet was effective in people that had had Type 2 diabetes for up to 10 years.
Both of these studies were very small, and were carried out in a research environment. We don't yet understand the long-term effects of these diets, or how a low-calorie diet might be used to bring about and maintain Type 2 diabetes remission in a real-life setting, as part of routine GP care.
What is the aim of the current research?
The DiRECT (Diabetes Remission Clinical Trial) study aims to find out if intensive weight control can bring about the remission of Type 2 diabetes and be maintained long-term through routine NHS care.
The trial will compare the long-term effects of a low-calorie diet and weight management programme to bsst available care for Type 2 diabetes.
What will the research involve?
A number of GP practices across Scotland and Tyneside are recruiting people aged 20-65 who are overweight and have been diagnosed with Type 2 diabetes in the last six years. Participants at half of the practices will receive the current best-available Type 2 diabetes care, while those at the other half will receive a low-calorie diet for between 8 and 20 weeks.
Afterwards, those on the low-calorie diet will be gradually re-introduced to normal food over a period of two to eight weeks and will receive expert support to help them maintain their weight loss in the long term.
Participants receiving best-available care will get weight loss support in accordance with the latest clinical guidelines, but won't receive the low-calorie diet.
The researchers will test metabolisms and measure fat deposits inside the body, to reveal exactly how major weight loss can put Type 2 diabetes into remission. They'll also carry out psychological assessments with the participants and healthcare professionals taking part in the study, to work out how this approach to weight management might form part of routine GP care.
Where is the research taking place?
This study will take place at around 30 GP practices in Scotland and Tyneside. The research will be carried out and the data analysed by researchers at the University of Glasgow and at Newcastle University.
Who can take part?
Only people invited to take part by their GP practice can get involved in this study. Recruitment is only taking place at selected GP practices in Scotland and Tyneside. Individual patients are not being recruited.
How will it benefit people with diabetes?
If this study shows that a low-calorie diet can safely put Type 2 diabetes into remission for the long-term, it could completely transform the way this condition is viewed and treated.
If the diet can be used practically and effectively, it could lead to significant changes in the way that Type 2 diabetes is managed by the NHS. It could also help people with this condition live for longer, improving quality of life and reducing the risk of serious health complications, without the need for invasive weight loss surgery.
If a low-calorie diet can be used within routine GP care , it could ultimately be of enormous benefit to millions of people living with Type 2 diabetes in the UK.
When will results be available?
This study will last until October 2018, and the overall results will be released once all of the data has been analysed. We'll report the results in Diabetes UK publications and on the website.
The low-calorie diet
What will the diet used consist of?
The diet used in DiRECT will last for between 8 and 20 weeks and provide around 800 calories a day. It will consist of four diet soups or shakes per day, providing all essential vitamins and minerals and lots of fluids.
Will the diet cure Type 2 diabetes?
The diet being studied isn't a 'quick fix' for Type 2 diabetes. It should help people taking part in the study to lose weight – specifically, the fat in and around their liver and pancreas. This should, in turn, help to put their Type 2 diabetes into remission.
It's likely that some people who take part in the research will find the diet challenging, and every participant will have to work hard to keep weight off in the long-term to maintain Type 2 diabetes remission.
Is the diet used in this research available now?
Low-calorie diet foods are not available on prescription from the NHS. They're marketed by a range of private companies, but can be expensive and come with limited evidence of long-term benefit.
This research is the only way to tell if weight management using a low-calorie diet is practical and more effective than the current best-available treatments for Type 2 diabetes.
Should people with Type 2 diabetes follow the diet used in this research?
Until we have evidence that a low-calorie diet is more effective than the current best-available treatment, Diabetes UK recommend that people with Type 2 diabetes only attempt to lose weight in this way after they have spoken to their GP.
We're confident that DiRECT will answer important questions and give the NHS enough evidence to decide whether low-calorie diets should be offered as a routine treatment option. People with diabetes should always consult their GP before making changes to the way that they manage their condition.
What diet does Diabetes UK recommend for people with Type 2?
Diabetes UK recommends that people with Type 2 diabetes eat a healthy, balanced diet that is low in sugar, salt and fat and includes plenty of fruits and vegetables. For information on living a healthy lifestyle and eating well with Type 2 diabetes please see our guide to diabetes.
Professor Roy Taylor at Newcastle University and Professor Mike Lean at the University of Glasgow are comparing the long-term effects of a new weight management approach to the best diabetes care currently available.
The aim is to find out if an intensive weight management plan can help people put their Type 2 diabetes into remission for the long term.
The DiRECT study
What is the background to this research?
Not everyone with Type 2 diabetes is overweight, but weight gain and obesity are the most important risk factors for Type 2 diabetes and the reason why Type 2 has become a global epidemic that affects overweight people of all ages.
Surgical operations, such as gastric banding and gastric bypass, are potential solutions because they lead to dramatic weight loss, which can put Type 2 diabetes into remission for up to 80% of patients. But these treatments are expensive, invasive and carry a risk of surgical complications, which mean they can only be offered as a last resort.
What do we know already about low-calorie diets?
In 2011, a Diabetes UK research trial at Newcastle University tested a low-calorie diet in 11 people with Type 2 diabetes, which helped us to understand how Type 2 diabetes can be put into remission.
After the 8-week diet, volunteers had reduced the amount of fat in their liver and pancreas. This helped to restore their insulin production and put their Type 2 diabetes into remission. Three months later, some had put weight back on, but most still had normal blood glucose control.
This study was only a first step. It was designed to tell us about the underlying biology of Type 2 diabetes, and it followed the participants for only three months.
Another study, published in 2016, confirmed these findings and showed (in 30 people) that Type 2 diabetes could be kept in remission 6 months after the low-calorie diet was completed. It also suggested that the diet was effective in people that had had Type 2 diabetes for up to 10 years.
Both of these studies were very small, and were carried out in a research environment. We don't yet understand the long-term effects of these diets, or how a low-calorie diet might be used to bring about and maintain Type 2 diabetes remission in a real-life setting, as part of routine GP care.
What is the aim of the current research?
The DiRECT (Diabetes Remission Clinical Trial) study aims to find out if intensive weight control can bring about the remission of Type 2 diabetes and be maintained long-term through routine NHS care.
The trial will compare the long-term effects of a low-calorie diet and weight management programme to bsst available care for Type 2 diabetes.
What will the research involve?
A number of GP practices across Scotland and Tyneside are recruiting people aged 20-65 who are overweight and have been diagnosed with Type 2 diabetes in the last six years. Participants at half of the practices will receive the current best-available Type 2 diabetes care, while those at the other half will receive a low-calorie diet for between 8 and 20 weeks.
Afterwards, those on the low-calorie diet will be gradually re-introduced to normal food over a period of two to eight weeks and will receive expert support to help them maintain their weight loss in the long term.
Participants receiving best-available care will get weight loss support in accordance with the latest clinical guidelines, but won't receive the low-calorie diet.
The researchers will test metabolisms and measure fat deposits inside the body, to reveal exactly how major weight loss can put Type 2 diabetes into remission. They'll also carry out psychological assessments with the participants and healthcare professionals taking part in the study, to work out how this approach to weight management might form part of routine GP care.
Where is the research taking place?
This study will take place at around 30 GP practices in Scotland and Tyneside. The research will be carried out and the data analysed by researchers at the University of Glasgow and at Newcastle University.
Who can take part?
Only people invited to take part by their GP practice can get involved in this study. Recruitment is only taking place at selected GP practices in Scotland and Tyneside. Individual patients are not being recruited.
How will it benefit people with diabetes?
If this study shows that a low-calorie diet can safely put Type 2 diabetes into remission for the long-term, it could completely transform the way this condition is viewed and treated.
If the diet can be used practically and effectively, it could lead to significant changes in the way that Type 2 diabetes is managed by the NHS. It could also help people with this condition live for longer, improving quality of life and reducing the risk of serious health complications, without the need for invasive weight loss surgery.
If a low-calorie diet can be used within routine GP care , it could ultimately be of enormous benefit to millions of people living with Type 2 diabetes in the UK.
When will results be available?
This study will last until October 2018, and the overall results will be released once all of the data has been analysed. We'll report the results in Diabetes UK publications and on the website.
The low-calorie diet
What will the diet used consist of?
The diet used in DiRECT will last for between 8 and 20 weeks and provide around 800 calories a day. It will consist of four diet soups or shakes per day, providing all essential vitamins and minerals and lots of fluids.
Will the diet cure Type 2 diabetes?
The diet being studied isn't a 'quick fix' for Type 2 diabetes. It should help people taking part in the study to lose weight – specifically, the fat in and around their liver and pancreas. This should, in turn, help to put their Type 2 diabetes into remission.
It's likely that some people who take part in the research will find the diet challenging, and every participant will have to work hard to keep weight off in the long-term to maintain Type 2 diabetes remission.
Is the diet used in this research available now?
Low-calorie diet foods are not available on prescription from the NHS. They're marketed by a range of private companies, but can be expensive and come with limited evidence of long-term benefit.
This research is the only way to tell if weight management using a low-calorie diet is practical and more effective than the current best-available treatments for Type 2 diabetes.
Should people with Type 2 diabetes follow the diet used in this research?
Until we have evidence that a low-calorie diet is more effective than the current best-available treatment, Diabetes UK recommend that people with Type 2 diabetes only attempt to lose weight in this way after they have spoken to their GP.
We're confident that DiRECT will answer important questions and give the NHS enough evidence to decide whether low-calorie diets should be offered as a routine treatment option. People with diabetes should always consult their GP before making changes to the way that they manage their condition.
What diet does Diabetes UK recommend for people with Type 2?
Diabetes UK recommends that people with Type 2 diabetes eat a healthy, balanced diet that is low in sugar, salt and fat and includes plenty of fruits and vegetables. For information on living a healthy lifestyle and eating well with Type 2 diabetes please see our guide to diabetes.
2016年7月4日星期一
FASTING: BACK TO THE FUTURE
Although the notion of electing to go without food for prolonged periods of time to improve one's health has not been something commonly considered in recent times, fasting has a long and important history. In fact, fasting played a vitally large part in early human survival. Fortunately, this ancient knowledge is making a dramatic comeback and is beginning to transform the way modern healthcare providers view their responsibilities to patients.
Human beings have the capability to survive extended periods of fasting. This was certainly known in our hunter-gatherer days, since many humans were forced to live through periods when little or no food was available to them. However, since the advent of agriculture and increasing technological advancement, modern humans have largely lost their awareness of this powerful, innate capability.
For example, the 1937 edition of The New Standard Encyclopedia stated that for humans, "Generally death occurs after eight days of deprivation of food." By 1956, this grim pronouncement inched somewhat closer to reality. That year's edition of the American Peoples Encyclopedia stated that survival time in men during water-only fasting ranged from 17 to 76 days.
In actuality, the "authorities" writing in these encyclopedias had no idea what they were talking about, but their conclusions are consistent with what most people might think. However, if we go back in time to earlier writings, we see that more "primitive" cultures were often more aware of the extent of our fasting capability. In the Bible, for example, Moses, David, Jesus, and Elijah were said to have fasted for up to 40 days.
Physiological Benefits of Fasting
Fasting can be thought of as a period of profound rest, during which time your body is free to rapidly undertake a wide variety of beneficial physiological activities, some of which are described below.
1. Neuroadaptation
Fasting helps your taste sensors adapt to a low salt intake. By allowing your body to "neuroadapt" to low-salt food, fasting rapidly facilitates the adoption of a health- promoting diet. This process of neuroadaptation appears to take place more rapidly during fasting than merely eating a low salt diet.
2. Enzymatic Recalibration
During fasting your body induces enzymatic changes that can affect numerous systems ranging from detoxification of endogenous and exogenous substances to the mobilization of fat, glycogen and protein reserves. These changes seem to persist after the fasting process, which may explain some of the dramatic clinical changes seen in patients after fasting.
3. Weight Loss
Although fasting is not generally recommended as a primary weight loss strategy, weight loss is a predictable consequence of fasting. Most people average a loss of approximately one pound per day over the course of a fast. (When weight loss is your primary concern, a health- promoting diet coupled with exercise is usually your best approach.)
4. Detoxification
Fasting is generally thought of as a tool to facilitate detoxification, promoting the mobilization and elimination of endogenous substances such as cholesterol and uric acid and exogenous substances such as dioxin, PCBs, and other toxic chemical residue.
5. Insulin Resistance
Fasting appears to have a profound effect on insulin resistance, which is thought to be intimately involved with diabetes and high blood pressure. When your body produces adequate insulin, but it is ineffective due to resistance at the cells in the liver and elsewhere, your blood sugar levels rise. This can lead to serious clinical consequences. Fortunately, after a period of fasting, this problem is often dramatically improved.
6. Natriuresis
Water-only fasting induces a powerful natriuretic effect, which allows the body to eliminate excess sodium and water from your body. This process allows for the resolution of chronic problems with edema and helps reduce the increased blood volume associated with high blood pressure.
7. Reducing Gut Leakage
When chronic inflammation involves the intestinal mucosa, a condition arises whereby small particles of incompletely digested foods can be absorbed into the blood stream. This introduction of foreign peptide molecules to the blood stream may stimulate an immunological cascade of effects collectively known as gut leakage. In genetically vulnerable individuals, gut leakage may be associated with the aggravation of numerous clinical entities including arthritis, colitis, asthma, allergies, and fatigue.
8. Sympathictonia
Hypersympathictonia (increased tone of the sympathetic nervous system) is thought to be associated with many problems ranging from digestive disturbances to anxiety disorders. Fasting appears to have a profound normalizing effect on the overall tone of the autonomic nervous system.
In all there are many mechanisms through which fasting may be having its profound effect. Further research into these and other areas should prove illuminating.
A Serendipitous Survival
In light of the clear misunderstanding of fasting by the medical profession, the unexpected, successful fasting experience of Henry Tanner, M.D., is truly remarkable. In 1877, Dr. Tanner was a respected, middle-aged physician living in Duluth, Minnesota. He had suffered for years with rheumatism and had consulted with seven fellow physicians, all of whom considered his case to be "hopeless." He also suffered from asthma, which chronically disrupted his sleep. He spent his waking hours in constant pain.
Tanner had been taught in medical school that humans could live only ten days without food and in this knowledge he found solace. Not believing in suicide, he determined that he would simply starve himself to death. As he stated later, "Life to me under the circumstances was not worth living... and I had made up my mind to rest from physical suffering in the arms of death." But fate had an agreeable surprise for Dr. Tanner. By unwittingly invoking a constellation of health-promoting responses associated with water-only fasting, he rapidly recovered.
By the fifth day of his fast, he was able to begin to sleep more peacefully. By the eleventh day, he reported feeling "as well as in my youthful days." Fully expecting that by this point he should be near death, he asked a fellow physician, Dr. Moyer, to examine him. Not surprisingly, Dr. Moyer was amazed.
According to Tanner's recollection, Moyer told him, "You ought to be at death's door, but you certainly look better than I ever saw you before." Henry Tanner continued to fast, under Dr. Moyer's supervision, for an additional 31 days, a total of 42 days in all.
When fellow physicians heard his story, which was sensationalized in the press, they responded with disbelief and intense criticism. Though widely rebuked as a fraud, Tanner at least had the last laugh. After his fast, Tanner had no symptoms of asthma, rheumatism, or chronic pain and lived a full life until he died at the age of ninety.
Human Fasting Capabilities
Many fasts of longer than 100 days have been documented in recent scientific literature, the longest of which was 368 days. At the TrueNorth Health Center in California, we routinely supervise water-only fasts of up to 40 days, and in certain circumstances, even longer.
In our experience, fasting has never been lethal and is often remarkably helpful. During our 20 years of supervising the care of more than 5,000 patients, fasting has proven to be both safe and effective. It has provided many patients a new lease on life.
Reawakening to an Ancient Truth
Throughout most of the 20th century, which witnessed a period of remarkable medical innovation in surgical techniques, radiation therapies, and new "miracle" drugs, the self-healing mechanisms that are unleashed during water-only fasting were largely unappreciated.
However, as the century drew to a close, something extraordinary began to occur. After decades of collective awe of modern medicine and its purveyors, a strong undercurrent of disillusionment began to appear. There came the beginnings of a philosophical revolution that would lead health science in a promising new direction.
This new direction centers on the realization that health and healing are best supported when the biological roots of our nature are understood and respected. This new philosophical approach is based on the awareness that health and healing are natural processes. As a result, the focus of attention has increasingly shifted away from the traditional medical emphasis on drugs and surgery toward an exploration of the circumstances and requirements necessary to unleash and enhance these natural processes.
Fortunately, unlike health problems in the past, including such phenomena as water-borne diseases, nutritional deficiencies, and epidemics of tuberculosis and pneumonia that at one time were confusing puzzles - our present day epidemics of obesity, heart disease, high blood pressure, diabetes and cancer are not nearly so mysterious. It is becoming increasingly clear that the majority of present day health problems are the result of modern dietary excesses.
Simply put, most of our health problems are the result of our eating too much of the wrong things. We ingest too much fat and protein (especially animal fat and animal protein); too much refined sugar and other refined carbohydrates; and too many drugs, including tobacco, coffee, tea, alcohol, and soda. It is not surprising that nearly 50% of American teenagers are overweight when you consider that the average teenager consumes 25% of his or her calories from soda pop.
In the face of the current unprecedented epidemics of disease caused by dietary excess, it is understandable that the ancient healing method of water-only fasting is beginning to make intuitive sense to many people. Going without food for a period of time provides the ultimate opportunity for the reversal of the consequences of dietary excess, a chance to let an overfed and overburdened body take steps to restore health.
Rest assured that the appeal of fasting is not based solely on mere intuition. With the recent publication of the first-ever large-scale study conducted on the use of water-only fasting with life-threatening illness, what was previously considered intuitive has become scientifically apparent. Water-only fasting offers extraordinary potential for health and healing, and for some conditions it appears to be the most effective treatment available.
Fasting and High Blood Pressure
High blood pressure (also known as hypertension) is the leading contributing cause of morbidity and mortality in industrialized societies, and is the leading reason for visits to doctors and for the use of prescription medication. It is diagnosed when a patient's pressures exceed 140/90 mm Hg. The human and financial costs of this condition are staggering.
In 1984, doctors at the TrueNorth Health Center began to investigate the use of fasting in the treatment of this devastating condition. Our study involved 174 high blood pressure patients, all of whom were admitted to the Center for treatment involving water-only fasting.
The results of the study were astonishing. Every patient experienced blood pressure reductions sufficient to eliminate the need for medication, and over ninety percent of patients achieved completely normal blood pressure. A stunning reduction of over 60 points in systolic (upper) blood pressure was noted in those patients with highly elevated pressures (known as Stage III Hypertension), where systolic pressures are greater than 180 mm Hg. These results represent the largest effect size ever shown in lowering blood pressure, and they are estimated to be five times the effect expected from medications alone.
With assistance from our colleagues at Cornell University, our study, "Medically Supervised Water-only Fasting in the Treatment of Hypertension" was completed and accepted for publication by the peer-reviewed and indexed Journal of Manipulative and Physiological Therapeutics. It appeared in the June, 2001 issue of JMPT.
A second study, also conducted at the Center, was recently accepted for publication in the Journal of Alternative and Complementary Medicine. In this investigation, we evaluated the effect of water-only fasting on 64 patients admitted with so-called "borderline" hypertension. These are individuals who have systolic blood pressures between 120 and 140 mm Hg.
Patients with blood pressures in this range are often led to believe that their blood pressures are "normal." For example, a patient with a systolic blood pressure of 138/88 would be considered "normal" by conventional medical standards, despite the fact that they are five times more likely to die from a heart attack or stroke than an individual who has a systolic blood pressure of 110 mm Hg. Sixty-eight percent of all deaths attributed to the effects of high blood pressure occur in individuals whose systolic blood pressure is in this range.
The patients in our second study had a mean reduction in systolic blood pressure of 20 mm Hg. The average patient in the study, beginning with a systolic blood pressure of nearly 130 mm Hg, ended his stay with systolic blood pressure of just below 109 mm Hg. This represents a very substantial improvement in health. As just stated, he is now five times less likely to die from a heart attack or stroke than he was before.
Fasting Studies Draw Attention
As a result of the publication of these studies, the fasting program at TrueNorth Health Center attracted the attention of the International Union of Operating Engineers (IUOE), a large, national labor union. In March 2001, the Center's residential health education program, including the supervision of water-only fasting, became a fully covered medical benefit for all union members and spouses who have high blood pressure or diabetes.
In conjunction with this association with IUOE, the doctors at the Center are conducting a third fasting study. It is a prospective study with long-term follow-up to evaluate the use of fasting in the treatment of high blood pressure and diabetes. We are looking not only at the clinical outcomes of the patients (improved health and reduced morbidity), but also the effect on long-term costs of care for the patients who undergo fasting compared to those who choose conventional medical care.
In conjunction with this association with IUOE, the doctors at the Center are conducting a third fasting study. It is a prospective study with long-term follow-up to evaluate the use of fasting in the treatment of high blood pressure and diabetes. We are looking not only at the clinical outcomes of the patients (improved health and reduced morbidity), but also the effect on long-term costs of care for the patients who undergo fasting compared to those who choose conventional medical care.
The initial results are outstanding. Based on data from the first group of subjects with one-year follow-ups, the average cost reduction for fasting patients compared to patients receiving conventional medical care appears to be substantial. Once a large enough number of patients have completed the program and the long-term outcomes are calculated, we expect to publish additional papers documenting what appears to be a tremendously cost effective approach to managing these high risk, high medical cost, high blood pressure and diabetes patients.
Hope for the Future
Hopefully, these results of the TrueNorth Health Center's studies will be a contributing force in both a philosophical and practical revolution in health care. With clear and convincing evidence to guide them, and substantial cost savings to motivate them, other unions and insurance companies may decide to encourage and support the use of fasting for those they serve. In doing so, they could make available to the millions of sick and suffering patients the most profound health rediscovery of our time: the understanding that fasting allows the body to heal itself without the risk and excess cost associated with conventional medical care and drug use.
Do You Need to Fast?
Throughout history, people have noticed that when they become acutely ill, they lose their appetites. The early Hygienic physicians reasoned that there must be some physiological reason for this loss of appetite. Through observation and experimentation, they discovered that fasting - the complete abstinence from all substances except pure water, in an environment of complete rest - allows the body to make a unique physiological adaptation.
In the fasting state, the duration and intensity of the symptoms of illness, such as inflammation, mucus production, fever, diarrhea, etc., are often dramatically reduced. Fasting has been found to be the most efficient and powerful means available to facilitate self-healing.
Further experimentation and observation found that fasting is also effective in the resolution of chronic disease. Chronic disease, including heart disease, diabetes, cancer, arthritis, respiratory illness, autoimmune disease, etc., can be the result of several different factors. These factors include inappropriate diet, such as the consumption of animal products and refined foods, the use of drugs, including tobacco, alcohol, coffee, etc., a lack of adequate sleep or exercise, or exposure to environmental stressors such as pollution, radiation, excess noise, etc., or excess psychological stress and hereditary factors.
Fasting is an important tool in resolving the symptoms of acute illness and chronic disease, but its benefits are not limited to dealing with symptoms.
Making the transition to healthful living
It is difficult to break habits and patterns of behavior established over many years. The typical Western lifestyle leads to taste buds acclimated to stimulating foods, muscles that are flabby, and a nervous system that depends on stimulatory drugs (such as caffeine) to keep it going despite a lack of sleep. Often, as people attempt to change their diets and lifestyles, they find healthful foods unappetizing, exercise painful, and the symptoms of withdrawal from stimulants unbearable. The slow process of detoxification that accompanies the cessation of bad habits can cause unpleasant symptoms that persist for weeks or months.
Speeding up the process
Fasting is a method of speeding up the detoxification process. It can be an intense and sometimes unpleasant experience, but it is highly effective. After fasting, healthful foods often taste delicious, and pernicious habits often have much less appeal. Fasting is the most efficient means available to overcome dependencies of a variety of drugs, including caffeine, nicotine, alcohol, marijuana and others. Educational programs available at institutions specializing in fasting supervision help people to develop the skills necessary to select and prepare healthful foods, develop a sensible exercise program, and find emotional support.
Overcoming signs of illness
Some individuals appear and feel healthy but still manifest abnormal signs, such as high blood pressure, elevated blood levels of cholesterol, triglycerides, glucose, uric acid, or liver enzymes, etc. Fasting is often extremely effective at allowing the body to eliminate the signs associated with disease.
Prevention
Many individuals have adopted a health-promoting diet and lifestyle to overcome disease. They may be completely free of all signs and symptoms of disease but choose to use fasting as a preventive measure to allow the body to eliminate the metabolic products that can accumulate within the cells of the body despite our best efforts. Fasting may offer its greatest potential in the prevention of disease. Fasting also can be used as a diagnostic tool in uncovering sub-clinical pathology that may exist.
Doing it right
Whether fasting is used in the transition to a healthful diet and lifestyle, to overcome the signs and symptoms of disease, or as a preventive measure, it is a powerful tool for helping sick people to get well and healthy people to stay healthy.
The most important advice about fasting is: Do it right or don't do it. Complete rest, a supportive environment, and professional supervision are required to ensure that fasting will be a safe and effective experience.
Case studies
The following case studies will give some insight into the many ways people can benefit from fasting.
J.W., a 36-year-old female, 5 feet 4 inches tall and 215 pounds, decided that she wanted to quit smoking, lose weight, overcome her "food addictions," and resolve a 15-year history of chronic constipation. She also suffered from severe back pain and sciatica. She had, in her own words, tried "everything," and in desperation came to the Center for Conservative Therapy's residential health care program on the advice of a friend who had undertaken a fast there two years earlier.
After her initial examination and two days of preparatory feeding, J.W. underwent a fast of 12 days. She experienced numerous symptoms during her fast but did not experience any significant craving for cigarettes despite her one-pack-per-day habit of over 20 years duration. She also did not experience any hunger after the second day of fasting. She did experience nausea, a foul taste in her mouth, headaches, and low back pain. After 12 days of fasting, J.W. underwent a 14-day re-feeding program. By the fourth day of re-feeding, she was having normal bowel movements for the first time in many years. She lost a total of 31 pounds. During her re-feeding time, she received chiropractic manipulation and physiotherapy for her joint dysfunction, in conjunction with instruction on stretching and proper body use. At the time of her release, she was free of sciatica and felt prepared to face the "real" world.
At her six-month follow-up, J.W. had managed to lose an additional 15 pounds, had successfully become an ardent non-smoker, had completely normal bowel function, and had remained free of back pain and sciatica.
M.T., a 46-year-old male, was suffering from macular degeneration [loss of central vision], high blood pressure, joint pain, and fatigue. Despite his efforts at making dietary changes, his symptoms continued to progress, which was upsetting to him. Blood pressure medications were only successful at reducing his blood pressure to 180/110, and they seemed to be interfering with his sexual function.
After three weeks of fasting and two weeks of re-feeding, M.T. was a "new" man. His blood pressure normalized without medications at 114/74, and his joint pain completely resolved. At his follow-up a year later, he reported no return of the visual problems from macular degeneration, and his blood pressure was 120/74.
S.S., a 34-year-old female, had been ill for several years. She had been previously diagnosed as having chronic fatigue immune deficiency syndrome, Epstein-Barr viral infection, and chronic candidiasis. She reported a history of depression, panic attacks, palpitations, and sleep disruption. She seemed sensitive to everything she ate, including fruits and vegetables.
S.S. underwent a fast with the hope of reducing her extreme hypersensitivity. Her fast was quite difficult, and after just 12 days it had to be discontinued due to extreme emotional volatility. She had a slow recovery, but within four months of her fast she reported substantial improvement. She was much less fatigued, was sleeping better, and could tolerate a wider variety of whole natural foods. S.S. will undergo another fast soon.
A.S., a 74-year-old female, had been diagnosed as having breast cancer 10 years ago. She had undergone a lumpectomy, but had refused all other medical treatment. Since then, she has been totally committed to healthful living and has been absolutely compliant with all the diet and lifestyle recommendations.
Once each year she comes to the Center for "preventive" fasting. She usually fasts for 10 days without significant symptoms. On her most recent fast, although she arrived feeling great, by the second day she had a fever of 101 degrees and was in extreme discomfort. It was not until the eighth day that her fever broke and she felt wonderful again. I believe that this represented a significant healing crisis, since all her laboratory results were within normal limits. She has had no recurrences of cancer and continues to do well.
2016年6月28日星期二
Fasting for Longevity: 9 Questions for Dr. Valter D. Longo
In the 12 years I’ve been researching longevity for Blue Zones, I’ve met dozens of great scientists. None, however, has a more convincing strategy to slow the aging process than Dr. Valter Longo. He’s an award-winning researcher, gerontology and biological sciences professor and director of the Longevity Institute at the University of Southern California. Here he reveals some of his discoveries:
1. You grew up in Molochio, one of the small towns in Italy known for its incredible longevity. Is there anything special about the traditional diet in Molochio?
1. You grew up in Molochio, one of the small towns in Italy known for its incredible longevity. Is there anything special about the traditional diet in Molochio?
Yes, there’s something called pasta e vaianeia, which is slang for pasta and green beans. When I was growing up in Molochio, we used to eat it about five times a week. And what it was is a little pasta and a ton of these green beans with the pod, and then other vegetables and olive oil. So I think that was the perfect meal because it has a little bit of everything. I remember we used to always complain, “Not again! Not this thing again!” But that’s all we ate all the time. These ingredients are from the foods that they had because they were poor and that’s all they could afford. Back in the day, the bread used to be this very dark, whole bread that was incredible. Those are some of the things I talk about in my book, which hopefully will be published before the end of the year. I think that the centenarians may have benefited from eating like this for decades and decades.
2. You’ve found that a low-protein diet is healthier for people. Can you tell us why?
2. You’ve found that a low-protein diet is healthier for people. Can you tell us why?
Yes, well it’s healthy for people before 70. In fact, a high protein diet is bad for you. Growth hormone pathways, including
TOR and IGF-1, are controlled by proteins and they are accelerators of the aging process. So, if you have a low-protein diet you might live longer and healthier.
3. Fasting comes with risks for some people. But you found that a certain type of fasting that you developed might favor longevity. Can you explain why?
Actually fasting itself, which allows water only, is very difficult for people to do. What we’ve done is develop a fasting mimicking diet, which is abbreviated as FMD. It was really the result of years of study with animals to try to figure how much we can add to the diet of someone before we lose the effects of fasting and what kind of ingredients to include. We came up with something that is low-protein, low sugar, and relatively high fat that does exactly that. Then, we tested it on mice and later in a human clinical trial. In the mouse study, we show that with fasting done only twice a month for four days these mice lived longer and have about half of the cancers. When they do develop cancer, they develop it later in life. Cognitive performance improved, they had less inflammation, and they lost fat specifically in the abdomen. Periodical fasting we really think is the way.
4. How often should the average person go on a fast?
4. How often should the average person go on a fast?
It depends. Somebody that is very healthy, exercises, has a Blue Zone diet, and has a perfect weight may need it twice a year. Somebody that has high fasting glucose, high blood pressure, abdominal adiposity (so they’re overweight or obese, etc.), or they have a high risk of cancer in the family, they probably need to do it once a month. Keep in mind that water only or similar fasting should only be done in clinics. ProLon, instead, because it provides more calories and was clinically tested, can be done at home with the approval of a doctor.
5. Tell me a little bit about your company. What is the experience like with ProLon?
5. Tell me a little bit about your company. What is the experience like with ProLon?
The product is called ProLon for pro-longevity. This is product and has been clinically tested on over 100 people with solid results. I started the company because when we first published research on fasting for cancer patients asked the same questions: “What can I eat?” Our research found that almost nobody could fast with water only, even if they had cancer. They cheated; they felt that it was just too hard. So we developed this fasting mimicking diet that allowed them to eat about half of the normal calories. I committed all my shares in L-Nutra to a nonprofit organization that I started called Create Cures, so we could continue to research and learn about fasting.
6. Can you describe some of the foods that people will be eating while on the five day fast?
6. Can you describe some of the foods that people will be eating while on the five day fast?
It contains vegetable soups, which you eat twice a day; olives, vegetable chips, nuts, bars made of nuts (all of them are low sugar, high nourishment). There are supplements that are specially developed to maximize nourishment. We also have drinks and teas that are basically mimicking what the body produces naturally during fasting. We include those for safety, in case the body dips too deeply into their reserves .
7. If a normal middle-aged person with normal health started fasting twice a year through his or her 50s, 60s, 70s, 80s – do you think that would add years to their life?
7. If a normal middle-aged person with normal health started fasting twice a year through his or her 50s, 60s, 70s, 80s – do you think that would add years to their life?
Every indication in mice and humans, says the answer is yes. And even if it didn’t add years to your life it will add healthy years to your life, so you’ll be healthier longer. It is pretty clear that you will have a reduction in the chance of getting a chronic disease.
8.Besides lowering our protein intake if we’re under 65 and fasting occasionally, what else you think people can do to add healthy years to their life?
8.Besides lowering our protein intake if we’re under 65 and fasting occasionally, what else you think people can do to add healthy years to their life?
I would say number one is nourishment. Make sure that you have everything your body needs, whether it is vitamin D or essential fatty acids, or iron, or zinc, or B12, etc. Those, combined with some weight training or resistance exercise so that you avoid losing muscle, are the essentials that I think will optimize somebody’s ability to stay healthy and also feel well.
9. Do you think that supplementation or certain drugs can help people live longer?
9. Do you think that supplementation or certain drugs can help people live longer?
I think it’s often a bad idea. For example, a drug called rapamycin slows aging, but it also causes hyperglycemia; it increases the blood glucose. We know that in mice it also increases cataracts and it increases testicular degeneration. It may also contribute to immunosuppression. Until we are completely sure these drugs and supplements are effective, but also very safe, it’s probably not a good idea.
禁食疗法：一年8天不吃饭 能提高免疫力
一年只需要禁食8天，就可以提高身体的免疫系统功能。这是美国一个研究小组针对禁食疗法的最新研究结果。现代意义上的禁食疗法起源于18世纪的欧洲，但实际上禁食的概念在中国道教的古老辟谷术以及其他一些世界性宗教中都有涉及。作为一种绿色的自然疗法，近年来，禁食疗法在许多欧美国家渐成风尚，中国民间也一直有人鼓吹禁食的好处。那么，除了提高免疫力之外，禁食疗法还有哪些神奇功效？如何科学地禁食？禁食有哪些风险和禁忌？带着这些问题，记者采访了有关专家。
禁食可再造免疫系统
英国《每日邮报》近日报道称，美国南加州大学研究者发表研究成果称，每年禁食8天就可以提高免疫系统功能。研究发现，禁食两天或两天以上即可有助于启动人体的免疫系统，尤其是当免疫系统因为衰老或接受癌症治疗而出现受损的情况下。研究者称，禁食会鼓励身体用新细胞取代旧的受损的细胞。
领导此研究的南加州大学长寿专家沃尔特·朗戈解释说：“当人挨饿时，人体系统会竭力节省能量，而节省能量的一个办法就是重复利用大量不被需要的免疫细胞，尤其是那些可能已经受损的免疫细胞。”
朗戈的小组发现，每半年禁食2~4天可以迫使身体调节到生存模式，消耗掉体内储存的脂肪和糖分，分解大量旧细胞。朗戈说，在禁食状态下，人体会发出信号，“命令”干细胞再造白细胞，重建整个免疫系统。“当身体免疫系统因为化疗或者衰老而被严重破坏时，可以说，通过禁食周期能够产生一个新的免疫系统。”
在试点试验中，研究者发现，如果癌症病人化疗前禁食72小时，那么就可以降低他们体内白细胞的受损程度。研究人员在摄入化疗药物的小鼠身上的试验还显示，禁食能降低化疗药物的副作用以及患癌小鼠的死亡率，而在老年小鼠身上的试验则显示，禁食可以提高其免疫力。这一研究成果发表在最新一期的《干细胞》上。
禁食疗法：
古已有之 欧洲重新兴起
禁食能提高身体免疫力？广州中山大学附属第一医院中医科主任教授、博士生导师秦鉴告诉记者，他和他的团队在研究中发现：禁食不但能让体内白细胞水平升高，从而杀灭肿瘤细胞和病毒，还可以降低炎症反应水平，调节身体对胰岛素的敏感性，不过，美国南加州大学的这一研究进一步揭示了其中的原理。
近年来，禁食疗法在欧洲兴起，成为一种减肥风尚，受到许多名人明星的追捧，并渐渐传入中国。禁食疗法通常是指在一定时间内，除了可以适量饮水、进食少量蔬菜汁、果汁外，禁止食用其他一切食物，仅仅依靠体内的能量储存保障生命活动的需要，以此来治疗或预防某些疾病。现代医学意义上的“禁食疗法”诞生于十八世纪的欧洲，但其实禁食(也称断食)与宗教修行有着密切关系。佛山市第一人民医院营养科主任医师潘文松指出，禁食疗法其实是借用了中国古代的辟谷疗法，辟谷作为道家的修炼术已经有几千年的历史，《黄帝内经》中亦有跟禁食疗法相关的记载。秦鉴则指出，中医养生学中自古就有禁食或饥饿疗法的概念，古人认为“欲要长生，腹中常清；欲人不死，肠中无滓”。
禁食是“无与伦比的自然疗法”？
潘文松说，目前国内中医界在做的禁食疗法研究显示，禁食疗法比较适合治疗高血压、高血脂、肥胖、糖尿病等代谢性疾病，这些病都是因为“吃得多，身体才出现问题”。秦鉴告诉记者，小到感冒，大到肿瘤，禁食疗法能治的病多达几十种。记者当天采访时重感冒初愈，秦鉴说像记者这种情况禁食两天就好了，根本不需要吃药打针，而通过禁食治感冒的方法早在《红楼梦》中晴雯伤风的章节就有提及。
秦鉴的团队在研究中发现，禁食疗法能治疗三类适应症，其中在治疗便秘、脂肪肝、高血压、脂代谢紊乱、肥胖和体重控制、骨性关节炎、风湿性关节炎、银屑病、睡眠呼吸暂停综合征等症时“效果非常好”。此外，禁食治疗在治疗II型糖尿病、代谢综合征、胃肠功能紊乱、肠易激综合征、暴食症、肌腱炎、过敏症、哮喘、背痛、支气管炎、念珠菌病、流感、憩室炎、枯草热、头痛等适应症方面效果也比较显著，“不能100%地保证治愈，但是可以让病况大大好转，而且可以重复治疗”。
秦鉴告诉记者，从中医角度讲，数天禁食可以去痰浊，令气机畅，脉络通，还能抑阴扶阳，有助于恢复人体的阴阳平衡。秦鉴说，除了各种病症的好转外，患者身体的整体状态提升了，普遍的反应是上楼梯不费力，身材变好，得到周围人的夸赞，情绪改善，能体验到愉快的感觉。
在秦鉴看来，作为自然疗法，禁食疗法是一种“无与伦比”的方法，简便，成本低，副作用小，一法多效，可以减少药物滥用。“中医是上工治未病，下工才是用药治，研究和推广中医禁食疗法是在往上工的方向走。”他预测，随着国人对健康问题的关注，未来10年之内禁食疗法会在国内掀起高潮。
禁食疗法Q&A
1.如何禁食？
秦鉴介绍说，禁食有两种，一种是限制一切物质进入胃肠道(包括水)的绝对禁食，而目前国际上一般采用相对禁食的方式，首先是不禁止水，其次是允许摄入少部分能量。秦鉴说，他在德国学习的禁食疗法是每天通过摄入果汁、蔬菜汁或牛奶、肉汤补充能量。而中山大学附属第一医院中医科目前采取的能量补充方法是向患者提供自制低热量餐包(每天400千卡以下)。
秦鉴小组提供的禁食疗法最长的周期需要9~11天，总共分三个阶段——缓冲期、禁食期、恢复期。在1~2天的缓冲期内，患者需要控制热量，逐步消除心理性饥饿，还要进行适量运动，将1500克水果分为三至四餐，喝2~3升矿泉水，此外还要戒茶、酒精和咖啡。在7天禁食期内，医护人员会用玄明粉、生理盐水为患者清洁肠道，还会根据保健或治疗疾病目的，让患者进行或不进行相关药物及餐包的补充，此外，患者还需要适量运动，补充水分。在1~2天的恢复期内，患者的饮食应当遵循从软到硬的步骤，逐步进入正常、均衡的营养膳食，食物中富含水果和蔬菜饮水。
2.禁食以多少天为宜？
潘文松认为，禁食少于三天没什么效果，有些人坚持一周一天的禁食方式，只是减少了总能量摄入，但是，人的体质只有在极端条件下才会改变，基因才会表达。
秦鉴对此不是很赞同，他认为禁食两天就可以起到治疗效果，这一禁食过程可以反复重复，直到达到自己的目标。他同时强调，除去前后的缓冲期和恢复期，禁食疗法一般应控制在7天以内，长了可能会对身体产生损害。
3.禁食有何风险和禁忌？
专家指出，禁食疗法尽管神奇，但是并非人人适用，而且一定要在医生指导下使用。有部分人体质不好，经受不了激烈的环境改变，尤其是心脏不好的人。他建议，心脏病患者、老年人不要尝试。
秦鉴指出，处于成长发育期的18岁以下青少年、身体免疫能力下降的70岁以上老年人以及处于怀孕、哺乳期的女性都不适合禁食治疗。此外，患有酒精中毒、阿尔茨海默症、神经性厌食、癫痫、广泛肿瘤、转移癌、艾滋病、肾功能衰竭、肺结核、精神分裂症的患者也不应进行禁食治疗。
4.禁食会不会把胃饿坏？
秦鉴说，当初他开始禁食疗法试验时，一些院内专家对其有所质疑，主要是担心对消化器官有影响。但其实，饿肚子不会把胃饿坏，因为所有因饥饿导致的疾病是人一直盼着有食物来，有了这种盼望的话，消化液会分泌得非常厉害。但是，如果一旦笃定这几天没有食物来了，胃酸的分泌很明显受到抑制。所以，住院病人在禁食期间，胃病不会犯的，因为他们知道有其他的能源供应，知道食物不会进到胃里去，所以胃液也不会分泌。
5.禁食跟辟谷有什么关系？
秦鉴说，辟谷跟科学相差较远，禁食是将辟谷科学化、世俗化，让没有经过任何修炼的人都可以尝试，而不仅仅限于修炼者。潘文松认为，辟谷是过去的修炼者在修炼过程中经历的自然过程，他们希望通过辟谷提高功力，增加心的宁静度，认为吃东西会导致浊气上升，要开发智慧或达到特异功能，就不能让饮食干扰身体。而现代意义上的禁食主要是从干细胞、肠道反应等科学研究进行理论支持。此外，禁食是短时间不吃东西，以激活体内的某些机能，禁食者今天还吃得饱饱的，明天就开始少吃或不吃东西了，但辟谷修炼者是整体上都少吃东西。
禁食可再造免疫系统
英国《每日邮报》近日报道称，美国南加州大学研究者发表研究成果称，每年禁食8天就可以提高免疫系统功能。研究发现，禁食两天或两天以上即可有助于启动人体的免疫系统，尤其是当免疫系统因为衰老或接受癌症治疗而出现受损的情况下。研究者称，禁食会鼓励身体用新细胞取代旧的受损的细胞。
领导此研究的南加州大学长寿专家沃尔特·朗戈解释说：“当人挨饿时，人体系统会竭力节省能量，而节省能量的一个办法就是重复利用大量不被需要的免疫细胞，尤其是那些可能已经受损的免疫细胞。”
朗戈的小组发现，每半年禁食2~4天可以迫使身体调节到生存模式，消耗掉体内储存的脂肪和糖分，分解大量旧细胞。朗戈说，在禁食状态下，人体会发出信号，“命令”干细胞再造白细胞，重建整个免疫系统。“当身体免疫系统因为化疗或者衰老而被严重破坏时，可以说，通过禁食周期能够产生一个新的免疫系统。”
在试点试验中，研究者发现，如果癌症病人化疗前禁食72小时，那么就可以降低他们体内白细胞的受损程度。研究人员在摄入化疗药物的小鼠身上的试验还显示，禁食能降低化疗药物的副作用以及患癌小鼠的死亡率，而在老年小鼠身上的试验则显示，禁食可以提高其免疫力。这一研究成果发表在最新一期的《干细胞》上。
禁食疗法：
古已有之 欧洲重新兴起
禁食能提高身体免疫力？广州中山大学附属第一医院中医科主任教授、博士生导师秦鉴告诉记者，他和他的团队在研究中发现：禁食不但能让体内白细胞水平升高，从而杀灭肿瘤细胞和病毒，还可以降低炎症反应水平，调节身体对胰岛素的敏感性，不过，美国南加州大学的这一研究进一步揭示了其中的原理。
近年来，禁食疗法在欧洲兴起，成为一种减肥风尚，受到许多名人明星的追捧，并渐渐传入中国。禁食疗法通常是指在一定时间内，除了可以适量饮水、进食少量蔬菜汁、果汁外，禁止食用其他一切食物，仅仅依靠体内的能量储存保障生命活动的需要，以此来治疗或预防某些疾病。现代医学意义上的“禁食疗法”诞生于十八世纪的欧洲，但其实禁食(也称断食)与宗教修行有着密切关系。佛山市第一人民医院营养科主任医师潘文松指出，禁食疗法其实是借用了中国古代的辟谷疗法，辟谷作为道家的修炼术已经有几千年的历史，《黄帝内经》中亦有跟禁食疗法相关的记载。秦鉴则指出，中医养生学中自古就有禁食或饥饿疗法的概念，古人认为“欲要长生，腹中常清；欲人不死，肠中无滓”。
禁食是“无与伦比的自然疗法”？
潘文松说，目前国内中医界在做的禁食疗法研究显示，禁食疗法比较适合治疗高血压、高血脂、肥胖、糖尿病等代谢性疾病，这些病都是因为“吃得多，身体才出现问题”。秦鉴告诉记者，小到感冒，大到肿瘤，禁食疗法能治的病多达几十种。记者当天采访时重感冒初愈，秦鉴说像记者这种情况禁食两天就好了，根本不需要吃药打针，而通过禁食治感冒的方法早在《红楼梦》中晴雯伤风的章节就有提及。
秦鉴的团队在研究中发现，禁食疗法能治疗三类适应症，其中在治疗便秘、脂肪肝、高血压、脂代谢紊乱、肥胖和体重控制、骨性关节炎、风湿性关节炎、银屑病、睡眠呼吸暂停综合征等症时“效果非常好”。此外，禁食治疗在治疗II型糖尿病、代谢综合征、胃肠功能紊乱、肠易激综合征、暴食症、肌腱炎、过敏症、哮喘、背痛、支气管炎、念珠菌病、流感、憩室炎、枯草热、头痛等适应症方面效果也比较显著，“不能100%地保证治愈，但是可以让病况大大好转，而且可以重复治疗”。
秦鉴告诉记者，从中医角度讲，数天禁食可以去痰浊，令气机畅，脉络通，还能抑阴扶阳，有助于恢复人体的阴阳平衡。秦鉴说，除了各种病症的好转外，患者身体的整体状态提升了，普遍的反应是上楼梯不费力，身材变好，得到周围人的夸赞，情绪改善，能体验到愉快的感觉。
在秦鉴看来，作为自然疗法，禁食疗法是一种“无与伦比”的方法，简便，成本低，副作用小，一法多效，可以减少药物滥用。“中医是上工治未病，下工才是用药治，研究和推广中医禁食疗法是在往上工的方向走。”他预测，随着国人对健康问题的关注，未来10年之内禁食疗法会在国内掀起高潮。
禁食疗法Q&A
1.如何禁食？
秦鉴介绍说，禁食有两种，一种是限制一切物质进入胃肠道(包括水)的绝对禁食，而目前国际上一般采用相对禁食的方式，首先是不禁止水，其次是允许摄入少部分能量。秦鉴说，他在德国学习的禁食疗法是每天通过摄入果汁、蔬菜汁或牛奶、肉汤补充能量。而中山大学附属第一医院中医科目前采取的能量补充方法是向患者提供自制低热量餐包(每天400千卡以下)。
秦鉴小组提供的禁食疗法最长的周期需要9~11天，总共分三个阶段——缓冲期、禁食期、恢复期。在1~2天的缓冲期内，患者需要控制热量，逐步消除心理性饥饿，还要进行适量运动，将1500克水果分为三至四餐，喝2~3升矿泉水，此外还要戒茶、酒精和咖啡。在7天禁食期内，医护人员会用玄明粉、生理盐水为患者清洁肠道，还会根据保健或治疗疾病目的，让患者进行或不进行相关药物及餐包的补充，此外，患者还需要适量运动，补充水分。在1~2天的恢复期内，患者的饮食应当遵循从软到硬的步骤，逐步进入正常、均衡的营养膳食，食物中富含水果和蔬菜饮水。
2.禁食以多少天为宜？
潘文松认为，禁食少于三天没什么效果，有些人坚持一周一天的禁食方式，只是减少了总能量摄入，但是，人的体质只有在极端条件下才会改变，基因才会表达。
秦鉴对此不是很赞同，他认为禁食两天就可以起到治疗效果，这一禁食过程可以反复重复，直到达到自己的目标。他同时强调，除去前后的缓冲期和恢复期，禁食疗法一般应控制在7天以内，长了可能会对身体产生损害。
3.禁食有何风险和禁忌？
专家指出，禁食疗法尽管神奇，但是并非人人适用，而且一定要在医生指导下使用。有部分人体质不好，经受不了激烈的环境改变，尤其是心脏不好的人。他建议，心脏病患者、老年人不要尝试。
秦鉴指出，处于成长发育期的18岁以下青少年、身体免疫能力下降的70岁以上老年人以及处于怀孕、哺乳期的女性都不适合禁食治疗。此外，患有酒精中毒、阿尔茨海默症、神经性厌食、癫痫、广泛肿瘤、转移癌、艾滋病、肾功能衰竭、肺结核、精神分裂症的患者也不应进行禁食治疗。
4.禁食会不会把胃饿坏？
秦鉴说，当初他开始禁食疗法试验时，一些院内专家对其有所质疑，主要是担心对消化器官有影响。但其实，饿肚子不会把胃饿坏，因为所有因饥饿导致的疾病是人一直盼着有食物来，有了这种盼望的话，消化液会分泌得非常厉害。但是，如果一旦笃定这几天没有食物来了，胃酸的分泌很明显受到抑制。所以，住院病人在禁食期间，胃病不会犯的，因为他们知道有其他的能源供应，知道食物不会进到胃里去，所以胃液也不会分泌。
5.禁食跟辟谷有什么关系？
秦鉴说，辟谷跟科学相差较远，禁食是将辟谷科学化、世俗化，让没有经过任何修炼的人都可以尝试，而不仅仅限于修炼者。潘文松认为，辟谷是过去的修炼者在修炼过程中经历的自然过程，他们希望通过辟谷提高功力，增加心的宁静度，认为吃东西会导致浊气上升，要开发智慧或达到特异功能，就不能让饮食干扰身体。而现代意义上的禁食主要是从干细胞、肠道反应等科学研究进行理论支持。此外，禁食是短时间不吃东西，以激活体内的某些机能，禁食者今天还吃得饱饱的，明天就开始少吃或不吃东西了，但辟谷修炼者是整体上都少吃东西。
2016年5月12日星期四
AN OLD IDEA, REVIVED: STARVE CANCER TO DEATH
In the early 20th century, the German biochemist Otto Warburg believed that tumors could be treated by disrupting their source of energy. Hisidea was dismissed for decades — until now.
The story of modern cancer research begins, somewhat improbably, with the sea urchin. In the first decade of the 20th century, the German biologist Theodor Boveri discovered that if he fertilized sea-urchin eggs with two sperm rather than one, some of the cells would end up with the wrong number of chromosomes and fail to develop properly. It was the era before modern genetics, but Boveri was aware that cancer cells, like the deformed sea urchin cells, had abnormal chromosomes; whatever caused cancer, he surmised, had something to do with chromosomes.
Today Boveri is celebrated for discovering the origins of cancer, but another German scientist, Otto Warburg, was studying sea-urchin eggs around the same time as Boveri. His research, too, was hailed as a major breakthrough in our understanding of cancer. But in the following decades, Warburg’s discovery would largely disappear from the cancer narrative, his contributions considered so negligible that they were left out of textbooks altogether.
Unlike Boveri, Warburg wasn’t interested in the chromosomes of sea-urchin eggs. Rather, Warburg was focused on energy, specifically on how the eggs fueled their growth. By the time Warburg turned his attention from sea-urchin cells to the cells of a rat tumor, in 1923, he knew that sea-urchin eggs increased their oxygen consumption significantly as they grew, so he expected to see a similar need for extra oxygen in the rat tumor. Instead, the cancer cells fueled their growth by swallowing up enormous amounts of glucose (blood sugar) and breaking it down without oxygen. The result made no sense. Oxygen-fueled reactions are a much more efficient way of turning food into energy, and there was plenty of oxygen available for the cancer cells to use. But when Warburg tested additional tumors, including ones from humans, he saw the same effect every time. The cancer cells were ravenous for glucose.
Warburg’s discovery, later named the Warburg effect, is estimated to occur in up to 80 percent of cancers. It is so fundamental to most cancers that a positron emission tomography (PET) scan, which has emerged as an important tool in the staging and diagnosis of cancer, works simply by revealing the places in the body where cells are consuming extra glucose. In many cases, the more glucose a tumor consumes, the worse a patient’s prognosis.
In the years following his breakthrough, Warburg became convinced that the Warburg effect occurs because cells are unable to use oxygen properly and that this damaged respiration is, in effect, the starting point of cancer. Well into the 1950s, this theory — which Warburg believed in until his death in 1970 but never proved — remained an important subject of debate within the field. And then, more quickly than anyone could have anticipated, the debate ended. In 1953, James Watson and Francis Crick pieced together the structure of the DNA molecule and set the stage for the triumph of molecular biology’s gene-centered approach to cancer. In the following decades, scientists came to regard cancer as a disease governed by mutated genes, which drive cells into a state of relentless division and proliferation. The metabolic catalysts that Warburg spent his career analyzing began to be referred to as “housekeeping enzymes” — necessary to keep a cell going but largely irrelevant to the deeper story of cancer.
“It was a stampede,” says Thomas Seyfried, a biologist at Boston College, of the move to molecular biology. “Warburg was dropped like a hot potato.” There was every reason to think that Warburg would remain at best a footnote in the history of cancer research. (As Dominic D’Agostino, an associate professor at the University of South Florida Morsani College of Medicine, told me, “The book that my students have to use for their cancer biology course has no mention of cancer metabolism.”) But over the past decade, and the past five years in particular, something unexpected happened: Those housekeeping enzymes have again become one of the most promising areas of cancer research. Scientists now wonder if metabolism could prove to be the long-sought “Achilles’ heel” of cancer, a common weak point in a disease that manifests itself in so many different forms.
There are typically many mutations in a single cancer. But there are a limited number of ways that the body can produce energy and support rapid growth. Cancer cells rely on these fuels in a way that healthy cells don’t. The hope of scientists at the forefront of the Warburg revival is that they will be able to slow — or even stop — tumors by disrupting one or more of the many chemical reactions a cell uses to proliferate, and, in the process, starve cancer cells of the nutrients they desperately need to grow.
Even James Watson, one of the fathers of molecular biology, is convinced that targeting metabolism is a more promising avenue in current cancer research than gene-centered approaches. At his office at the Cold Spring Harbor Laboratory in Long Island, Watson, 88, sat beneath one of the original sketches of the DNA molecule and told me that locating the genes that cause cancer has been “remarkably unhelpful” — the belief that sequencing your DNA is going to extend your life “a cruel illusion.” If he were going into cancer research today, Watson said, he would study biochemistry rather than molecular biology.
“I never thought, until about two months ago, I’d ever have to learn the Krebs cycle,” he said, referring to the reactions, familiar to most high-school biology students, by which a cell powers itself. “Now I realize I have to.”
Born in 1883 into the illustrious Warburg family, Otto Warburg was raised to be a science prodigy. His father, Emil, was one of Germany’s leading physicists, and many of the world’s greatest physicists and chemists, including Albert Einstein and Max Planck, were friends of the family. (When Warburg enlisted in the military during World War I, Einstein sent him a letter urging him to come home for the sake of science.) Those men had explained the mysteries of the universe with a handful of fundamental laws, and the young Warburg came to believe he could bring that same elegant simplicity and clarity to the workings of life. Long before his death, Warburg was considered perhaps the greatest biochemist of the 20th century, a man whose research was vital to our understanding not only of cancer but also of respiration and photosynthesis. In 1931 he won the Nobel Prize for his work on respiration, and he was considered for the award on two other occasions — each time for a different discovery. Records indicate that he would have won in 1944, had the Nazis not forbidden the acceptance of the Nobel by German citizens.
That Warburg was able to live in Germany and continue his research throughout World War II, despite having Jewish ancestry and most likely being gay, speaks to the German obsession with cancer in the first half of the 20th century. At the time, cancer was more prevalent in Germany than in almost any other nation. According to the Stanford historian Robert Proctor, by the 1920s Germany’s escalating cancer rates had become a “major scandal.” A number of top Nazis, including Hitler, are believed to have harbored a particular dread of the disease; Hitler and Joseph Goebbels took the time to discuss new advances in cancer research in the hours leading up to the Nazi invasion of the Soviet Union. Whether Hitler was personally aware of Warburg’s research is unknown, but one of Warburg’s former colleagues wrote that several sources told him that “Hitler’s entourage” became convinced that “Warburg was the only scientist who offered a serious hope of producing a cure for cancer one day.”
Although many Jewish scientists fled Germany during the 1930s, Warburg chose to remain. According to his biographer, the Nobel Prize-winning biochemist Hans Krebs, who worked in Warburg’s lab, “science was the dominant emotion” of Warburg’s adult life, “virtually subjugating all other emotions.” In Krebs’s telling, Warburg spent years building a small team of specially trained technicians who knew how to run his experiments, and he feared that his mission to defeat cancer would be set back significantly if he had to start over. But after the war, Warburg fired all the technicians, suspecting that they had reported his criticisms of the Third Reich to the Gestapo. Warburg’s reckless decision to stay in Nazi Germany most likely came down to his astonishing ego. (Upon learning he had won the Nobel Prize, Warburg’s response was, “It’s high time.”)
“Modesty was not a virtue of Otto Warburg,” says George Klein, a 90-year-old cancer researcher at the Karolinska Institute in Sweden. As a young man, Klein was asked to send cancer cells to Warburg’s lab. A number of years later, Klein’s boss approached Warburg for a recommendation on Klein’s behalf. “George Klein has made a very important contribution to cancer research,” Warburg wrote. “He has sent me the cells with which I have solved the cancer problem.” Klein also recalls the lecture Warburg gave in Stockholm in 1950 at the 50th anniversary of the Nobel Prize. Warburg drew four diagrams on a blackboard explaining the Warburg effect, and then told the members of the audience that they represented all that they needed to know about the biochemistry of cancer.
Warburg was so monumentally stubborn that he refused to use the word “mitochondria,” even after it had been widely accepted as the name for the tiny structures that power cells. Instead Warburg persisted in calling them “grana,” the term he came up with when he identified those structures as the site of cellular respiration. Few things would have been more upsetting to him than the thought of Nazi thugs chasing him out of the beautiful Berlin institute, modeled after a country manor and built specifically for him. After the war, the Russians approached Warburg and offered to erect a new institute in Moscow. Klein recalls that Warburg told them with great pride that both Hitler and Stalin had failed to move him. As Warburg explained to his sister: “Ich war vor Hitler da” — “I was here before Hitler.”
Imagine two engines, the one being driven by complete and the other by incomplete combustion of coal,” Warburg wrote in 1956, responding to a criticism of his hypothesis that cancer is a problem of energy. “A man who knows nothing at all about engines, their structure and their purpose may discover the difference. He may, for example, smell it.”
The “complete combustion,” in Warburg’s analogy, is respiration. The “incomplete combustion,” turning nutrients into energy without oxygen, is known as fermentation. Fermentation provides a useful backup when oxygen can’t reach cells quickly enough to keep up with demand. (Our muscle cells turn to fermentation during intense exercise.) Warburg thought that defects prevent cancer cells from being able to use respiration, but scientists now widely agree that this is wrong. A growing tumor can be thought of as a construction site, and as today’s researchers explain it, the Warburg effect opens the gates for more and more trucks to deliver building materials (in the form of glucose molecules) to make “daughter” cells.
If this theory can explain the “why” of the Warburg effect, it still leaves the more pressing question of what, exactly, sets a cell on the path to the Warburg effect and cancer. Scientists at several of the nation’s top cancer hospitals have spearheaded the Warburg revival, in hopes of finding the answer. These researchers, typically molecular biologists by training, have turned to metabolism and the Warburg effect because their own research led each of them to the same conclusion: A number of the cancer-causing genes that have long been known for their role in cell division also regulate cells’ consumption of nutrients.
Craig Thompson, the president and chief executive of the Memorial Sloan Kettering Cancer Center, has been among the most outspoken proponents of this renewed focus on metabolism. In Thompson’s analogy, the Warburg effect can be thought of as a social failure: a breakdown of the nutrient-sharing agreement that single-celled organisms signed when they joined forces to become multicellular organisms. His research showed that cells need to receive instructions from other cells to eat, just as they require instructions from other cells to divide. Thompson hypothesized that if he could identify the mutations that lead a cell to eat more glucose than it should, it would go a long way toward explaining how the Warburg effect and cancer begin. But Thompson’s search for those mutations didn’t lead to an entirely new discovery. Instead, it led him to AKT, a gene already well known to molecular biologists for its role in promoting cell division. Thompson now believes AKT plays an even more fundamental role in metabolism.
The protein created by AKT is part of a chain of signaling proteins that is mutated in up to 80 percent of all cancers. Thompson says that once these proteins go into overdrive, a cell no longer worries about signals from other cells to eat; it instead stuffs itself with glucose. Thompson discovered he could induce the “full Warburg effect” simply by placing an activated AKT protein into a normal cell. When that happens, Thompson says, the cells begin to do what every single-celled organism will do in the presence of food: eat as much as it can and make as many copies of itself as possible. When Thompson presents his research to high-school students, he shows them a slide of mold spreading across a piece of bread. The slide’s heading — “Everyone’s first cancer experiment” — recalls Warburg’s observation that cancer cells will carry out fermentation at almost the same rate of wildly growing yeasts.
Just as Thompson has redefined the role of AKT, Chi Van Dang, director of the Abramson Cancer Center at the University of Pennsylvania, has helped lead the cancer world to an appreciation of how one widely studied gene can profoundly influence a tumor’s metabolism. In 1997, Dang became one of the first scientists to connect molecular biology to the science of cellular metabolism when he demonstrated that MYC — a so-called regulator gene well known for its role in cell proliferation — directly targets an enzyme that can turn on the Warburg effect. Dang recalls that other researchers were skeptical of his interest in a housekeeping enzyme, but he stuck with it because he came to appreciate something critical: Cancer cells can’t stop eating.
Unlike healthy cells, growing cancer cells are missing the internal feedback loops that are designed to conserve resources when food isn’t available. They’re “addicted to nutrients,” Dang says; when they can’t consume enough, they begin to die. The addiction to nutrients explains why changes to metabolic pathways are so common and tend to arise first as a cell progresses toward cancer: It’s not that other types of alterations can’t arise first, but rather that, when they do, the incipient tumors lack the access to the nutrients they need to grow. Dang uses the analogy of a work crew trying to put up a building. “If you don’t have enough cement, and you try to put a lot of bricks together, you’re going to collapse,” he says.
Metabolism-centered therapies have produced some tantalizing successes. Agios Pharmaceuticals, a company co-founded by Thompson, is now testing a drug that treats cases of acute myelogenous leukemia that have been resistant to other therapies by inhibiting the mutated versions of the metabolic enzyme IDH 2. In clinical trials of the Agios drug, nearly 40 percent of patients who carry these mutations are experiencing at least partial remissions.
Researchers working in a lab run by Peter Pedersen, a professor of biochemistry at Johns Hopkins, discovered that a compound known as 3-bromopyruvate can block energy production in cancer cells and, at least in rats and rabbits, wipe out advanced liver cancer. (Trials of the drug have yet to begin.) At Penn, Dang and his colleagues are now trying to block multiple metabolic pathways at the same time. In mice, this two-pronged approach has been able to shrink some tumors without debilitating side effects. Dang says the hope is not necessarily to find a cure but rather to keep cancer at bay in a “smoldering quiet state,” much as patients treat their hypertension.
Warburg, too, appreciated that a tumor’s dependence upon a steady flow of nutrients might eventually prove to be its fatal weakness. Long after his initial discovery of the Warburg effect, he continued to research the enzymes involved in fermentation and to explore the possibility of blocking the process in cancer cells. The challenge Warburg faced then is the same one that metabolism researchers face today: Cancer is an incredibly persistent foe. Blocking one metabolic pathway has been shown to slow down and even stop tumor growth in some cases, but tumors tend to find another way. “You block glucose, they use glutamine,” Dang says, in reference to another primary fuel used by cancers. “You block glucose and glutamine, they might be able to use fatty acids. We don’t know yet.”
Given Warburg’s own story of historical neglect, it’s fitting that what may turn out to be one of the most promising cancer metabolism drugs has been sitting in plain sight for decades. That drug, metformin, is already widely prescribed to decrease the glucose in the blood of diabetics (76.9 million metformin prescriptions were filled in the United States in 2014). In the years ahead, it’s likely to be used to treat — or at least to prevent — some cancers. Because metformin can influence a number of metabolic pathways, the precise mechanism by which it achieves its anticancer effects remains a source of debate. But the results of numerous epidemiological studies have been striking. Diabetics taking metformin seem to be significantly less likely to develop cancer than diabetics who don’t — and significantly less likely to die from the disease when they do.
Near the end of his life, Warburg grew obsessed with his diet. He believed that most cancer was preventable and thought that chemicals added to food and used in agriculture could cause tumors by interfering with respiration. He stopped eating bread unless it was baked in his own home. He would drink milk only if it came from a special herd of cows, and used a centrifuge at his lab to make his cream and butter.
Warburg’s personal diet is unlikely to become a path to prevention. But the Warburg revival has allowed researchers to develop a hypothesis for how the diets that are linked to our obesity and diabetes epidemics — specifically, sugar-heavy diets that can result in permanently elevated levels of the hormone insulin — may also be driving cells to the Warburg effect and cancer.
The insulin hypothesis can be traced to the research of Lewis Cantley, the director of the Meyer Cancer Center at Weill Cornell Medical College. In the 1980s, Cantley discovered how insulin, which is released by the pancreas and tells cells to take up glucose, influences what happens inside a cell. Cantley now refers to insulin and a closely related hormone, IGF-1 (insulinlike growth factor 1), as “the champion” activators of metabolic proteins linked to cancer. He’s beginning to see evidence, he says, that in some cases, “it really is insulin itself that’s getting the tumor started.” One way to think about the Warburg effect, says Cantley, is as the insulin, or IGF-1, signaling pathway “gone awry — it’s cells behaving as though insulin were telling it to take up glucose all the time and to grow.” Cantley, who avoids eating sugar as much as he can, is currently studying the effects of diet on mice that have the mutations that are commonly found in colorectal and other cancers. He says that the effects of a sugary diet on colorectal, breast and other cancer models “looks very impressive” and “rather scary.”
Elevated insulin is also strongly associated with obesity, which is expected soon to overtake smoking as the leading cause of preventable cancer. Cancers linked to obesity and diabetes have more receptors for insulin and IGF-1, and people with defective IGF-1 receptors appear to be nearly immune to cancer. Retrospective studies, which look back at patient histories, suggest that many people who develop colorectal, pancreatic or breast cancer have elevated insulin levels before diagnosis. It’s perhaps not entirely surprising, then, that when researchers want to grow breast-cancer cells in the lab, they add insulin to the tissue culture. When they remove the insulin, the cancer cells die.
“I think there’s no doubt that insulin is pro-cancer,” Watson says, with respect to the link between obesity, diabetes and cancer. “It’s as good a hypothesis as we have now.” Watson takes metformin for cancer prevention; among its many effects, metformin works to lower insulin levels. Not every cancer researcher, however, is convinced of the role of insulin and IGF-1 in cancer. Robert Weinberg, a researcher at M.I.T.’s Whitehead Institute who pioneered the discovery of cancer-causing genes in the ’80s, has remained somewhat cool to certain aspects of the cancer-metabolism revival. Weinberg says that there isn’t yet enough evidence to know whether the levels of insulin and IGF-1 present in obese people are sufficient to trigger the Warburg effect. “It’s a hypothesis,” Weinberg says. “I don’t know if it’s right or wrong.”
During Warburg’s lifetime, insulin’s effects on metabolic pathways were even less well understood. But given his ego, it’s highly unlikely that he would have considered the possibility that anything other than damaged respiration could cause cancer. He died sure that he was right about the disease. Warburg framed a quote from Max Planck and hung it above his desk: “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die.”
The story of modern cancer research begins, somewhat improbably, with the sea urchin. In the first decade of the 20th century, the German biologist Theodor Boveri discovered that if he fertilized sea-urchin eggs with two sperm rather than one, some of the cells would end up with the wrong number of chromosomes and fail to develop properly. It was the era before modern genetics, but Boveri was aware that cancer cells, like the deformed sea urchin cells, had abnormal chromosomes; whatever caused cancer, he surmised, had something to do with chromosomes.
Today Boveri is celebrated for discovering the origins of cancer, but another German scientist, Otto Warburg, was studying sea-urchin eggs around the same time as Boveri. His research, too, was hailed as a major breakthrough in our understanding of cancer. But in the following decades, Warburg’s discovery would largely disappear from the cancer narrative, his contributions considered so negligible that they were left out of textbooks altogether.
Unlike Boveri, Warburg wasn’t interested in the chromosomes of sea-urchin eggs. Rather, Warburg was focused on energy, specifically on how the eggs fueled their growth. By the time Warburg turned his attention from sea-urchin cells to the cells of a rat tumor, in 1923, he knew that sea-urchin eggs increased their oxygen consumption significantly as they grew, so he expected to see a similar need for extra oxygen in the rat tumor. Instead, the cancer cells fueled their growth by swallowing up enormous amounts of glucose (blood sugar) and breaking it down without oxygen. The result made no sense. Oxygen-fueled reactions are a much more efficient way of turning food into energy, and there was plenty of oxygen available for the cancer cells to use. But when Warburg tested additional tumors, including ones from humans, he saw the same effect every time. The cancer cells were ravenous for glucose.
Warburg’s discovery, later named the Warburg effect, is estimated to occur in up to 80 percent of cancers. It is so fundamental to most cancers that a positron emission tomography (PET) scan, which has emerged as an important tool in the staging and diagnosis of cancer, works simply by revealing the places in the body where cells are consuming extra glucose. In many cases, the more glucose a tumor consumes, the worse a patient’s prognosis.
In the years following his breakthrough, Warburg became convinced that the Warburg effect occurs because cells are unable to use oxygen properly and that this damaged respiration is, in effect, the starting point of cancer. Well into the 1950s, this theory — which Warburg believed in until his death in 1970 but never proved — remained an important subject of debate within the field. And then, more quickly than anyone could have anticipated, the debate ended. In 1953, James Watson and Francis Crick pieced together the structure of the DNA molecule and set the stage for the triumph of molecular biology’s gene-centered approach to cancer. In the following decades, scientists came to regard cancer as a disease governed by mutated genes, which drive cells into a state of relentless division and proliferation. The metabolic catalysts that Warburg spent his career analyzing began to be referred to as “housekeeping enzymes” — necessary to keep a cell going but largely irrelevant to the deeper story of cancer.
“It was a stampede,” says Thomas Seyfried, a biologist at Boston College, of the move to molecular biology. “Warburg was dropped like a hot potato.” There was every reason to think that Warburg would remain at best a footnote in the history of cancer research. (As Dominic D’Agostino, an associate professor at the University of South Florida Morsani College of Medicine, told me, “The book that my students have to use for their cancer biology course has no mention of cancer metabolism.”) But over the past decade, and the past five years in particular, something unexpected happened: Those housekeeping enzymes have again become one of the most promising areas of cancer research. Scientists now wonder if metabolism could prove to be the long-sought “Achilles’ heel” of cancer, a common weak point in a disease that manifests itself in so many different forms.
There are typically many mutations in a single cancer. But there are a limited number of ways that the body can produce energy and support rapid growth. Cancer cells rely on these fuels in a way that healthy cells don’t. The hope of scientists at the forefront of the Warburg revival is that they will be able to slow — or even stop — tumors by disrupting one or more of the many chemical reactions a cell uses to proliferate, and, in the process, starve cancer cells of the nutrients they desperately need to grow.
Even James Watson, one of the fathers of molecular biology, is convinced that targeting metabolism is a more promising avenue in current cancer research than gene-centered approaches. At his office at the Cold Spring Harbor Laboratory in Long Island, Watson, 88, sat beneath one of the original sketches of the DNA molecule and told me that locating the genes that cause cancer has been “remarkably unhelpful” — the belief that sequencing your DNA is going to extend your life “a cruel illusion.” If he were going into cancer research today, Watson said, he would study biochemistry rather than molecular biology.
“I never thought, until about two months ago, I’d ever have to learn the Krebs cycle,” he said, referring to the reactions, familiar to most high-school biology students, by which a cell powers itself. “Now I realize I have to.”
Born in 1883 into the illustrious Warburg family, Otto Warburg was raised to be a science prodigy. His father, Emil, was one of Germany’s leading physicists, and many of the world’s greatest physicists and chemists, including Albert Einstein and Max Planck, were friends of the family. (When Warburg enlisted in the military during World War I, Einstein sent him a letter urging him to come home for the sake of science.) Those men had explained the mysteries of the universe with a handful of fundamental laws, and the young Warburg came to believe he could bring that same elegant simplicity and clarity to the workings of life. Long before his death, Warburg was considered perhaps the greatest biochemist of the 20th century, a man whose research was vital to our understanding not only of cancer but also of respiration and photosynthesis. In 1931 he won the Nobel Prize for his work on respiration, and he was considered for the award on two other occasions — each time for a different discovery. Records indicate that he would have won in 1944, had the Nazis not forbidden the acceptance of the Nobel by German citizens.
That Warburg was able to live in Germany and continue his research throughout World War II, despite having Jewish ancestry and most likely being gay, speaks to the German obsession with cancer in the first half of the 20th century. At the time, cancer was more prevalent in Germany than in almost any other nation. According to the Stanford historian Robert Proctor, by the 1920s Germany’s escalating cancer rates had become a “major scandal.” A number of top Nazis, including Hitler, are believed to have harbored a particular dread of the disease; Hitler and Joseph Goebbels took the time to discuss new advances in cancer research in the hours leading up to the Nazi invasion of the Soviet Union. Whether Hitler was personally aware of Warburg’s research is unknown, but one of Warburg’s former colleagues wrote that several sources told him that “Hitler’s entourage” became convinced that “Warburg was the only scientist who offered a serious hope of producing a cure for cancer one day.”
Although many Jewish scientists fled Germany during the 1930s, Warburg chose to remain. According to his biographer, the Nobel Prize-winning biochemist Hans Krebs, who worked in Warburg’s lab, “science was the dominant emotion” of Warburg’s adult life, “virtually subjugating all other emotions.” In Krebs’s telling, Warburg spent years building a small team of specially trained technicians who knew how to run his experiments, and he feared that his mission to defeat cancer would be set back significantly if he had to start over. But after the war, Warburg fired all the technicians, suspecting that they had reported his criticisms of the Third Reich to the Gestapo. Warburg’s reckless decision to stay in Nazi Germany most likely came down to his astonishing ego. (Upon learning he had won the Nobel Prize, Warburg’s response was, “It’s high time.”)
“Modesty was not a virtue of Otto Warburg,” says George Klein, a 90-year-old cancer researcher at the Karolinska Institute in Sweden. As a young man, Klein was asked to send cancer cells to Warburg’s lab. A number of years later, Klein’s boss approached Warburg for a recommendation on Klein’s behalf. “George Klein has made a very important contribution to cancer research,” Warburg wrote. “He has sent me the cells with which I have solved the cancer problem.” Klein also recalls the lecture Warburg gave in Stockholm in 1950 at the 50th anniversary of the Nobel Prize. Warburg drew four diagrams on a blackboard explaining the Warburg effect, and then told the members of the audience that they represented all that they needed to know about the biochemistry of cancer.
Warburg was so monumentally stubborn that he refused to use the word “mitochondria,” even after it had been widely accepted as the name for the tiny structures that power cells. Instead Warburg persisted in calling them “grana,” the term he came up with when he identified those structures as the site of cellular respiration. Few things would have been more upsetting to him than the thought of Nazi thugs chasing him out of the beautiful Berlin institute, modeled after a country manor and built specifically for him. After the war, the Russians approached Warburg and offered to erect a new institute in Moscow. Klein recalls that Warburg told them with great pride that both Hitler and Stalin had failed to move him. As Warburg explained to his sister: “Ich war vor Hitler da” — “I was here before Hitler.”
Imagine two engines, the one being driven by complete and the other by incomplete combustion of coal,” Warburg wrote in 1956, responding to a criticism of his hypothesis that cancer is a problem of energy. “A man who knows nothing at all about engines, their structure and their purpose may discover the difference. He may, for example, smell it.”
The “complete combustion,” in Warburg’s analogy, is respiration. The “incomplete combustion,” turning nutrients into energy without oxygen, is known as fermentation. Fermentation provides a useful backup when oxygen can’t reach cells quickly enough to keep up with demand. (Our muscle cells turn to fermentation during intense exercise.) Warburg thought that defects prevent cancer cells from being able to use respiration, but scientists now widely agree that this is wrong. A growing tumor can be thought of as a construction site, and as today’s researchers explain it, the Warburg effect opens the gates for more and more trucks to deliver building materials (in the form of glucose molecules) to make “daughter” cells.
If this theory can explain the “why” of the Warburg effect, it still leaves the more pressing question of what, exactly, sets a cell on the path to the Warburg effect and cancer. Scientists at several of the nation’s top cancer hospitals have spearheaded the Warburg revival, in hopes of finding the answer. These researchers, typically molecular biologists by training, have turned to metabolism and the Warburg effect because their own research led each of them to the same conclusion: A number of the cancer-causing genes that have long been known for their role in cell division also regulate cells’ consumption of nutrients.
Craig Thompson, the president and chief executive of the Memorial Sloan Kettering Cancer Center, has been among the most outspoken proponents of this renewed focus on metabolism. In Thompson’s analogy, the Warburg effect can be thought of as a social failure: a breakdown of the nutrient-sharing agreement that single-celled organisms signed when they joined forces to become multicellular organisms. His research showed that cells need to receive instructions from other cells to eat, just as they require instructions from other cells to divide. Thompson hypothesized that if he could identify the mutations that lead a cell to eat more glucose than it should, it would go a long way toward explaining how the Warburg effect and cancer begin. But Thompson’s search for those mutations didn’t lead to an entirely new discovery. Instead, it led him to AKT, a gene already well known to molecular biologists for its role in promoting cell division. Thompson now believes AKT plays an even more fundamental role in metabolism.
The protein created by AKT is part of a chain of signaling proteins that is mutated in up to 80 percent of all cancers. Thompson says that once these proteins go into overdrive, a cell no longer worries about signals from other cells to eat; it instead stuffs itself with glucose. Thompson discovered he could induce the “full Warburg effect” simply by placing an activated AKT protein into a normal cell. When that happens, Thompson says, the cells begin to do what every single-celled organism will do in the presence of food: eat as much as it can and make as many copies of itself as possible. When Thompson presents his research to high-school students, he shows them a slide of mold spreading across a piece of bread. The slide’s heading — “Everyone’s first cancer experiment” — recalls Warburg’s observation that cancer cells will carry out fermentation at almost the same rate of wildly growing yeasts.
Just as Thompson has redefined the role of AKT, Chi Van Dang, director of the Abramson Cancer Center at the University of Pennsylvania, has helped lead the cancer world to an appreciation of how one widely studied gene can profoundly influence a tumor’s metabolism. In 1997, Dang became one of the first scientists to connect molecular biology to the science of cellular metabolism when he demonstrated that MYC — a so-called regulator gene well known for its role in cell proliferation — directly targets an enzyme that can turn on the Warburg effect. Dang recalls that other researchers were skeptical of his interest in a housekeeping enzyme, but he stuck with it because he came to appreciate something critical: Cancer cells can’t stop eating.
Unlike healthy cells, growing cancer cells are missing the internal feedback loops that are designed to conserve resources when food isn’t available. They’re “addicted to nutrients,” Dang says; when they can’t consume enough, they begin to die. The addiction to nutrients explains why changes to metabolic pathways are so common and tend to arise first as a cell progresses toward cancer: It’s not that other types of alterations can’t arise first, but rather that, when they do, the incipient tumors lack the access to the nutrients they need to grow. Dang uses the analogy of a work crew trying to put up a building. “If you don’t have enough cement, and you try to put a lot of bricks together, you’re going to collapse,” he says.
Metabolism-centered therapies have produced some tantalizing successes. Agios Pharmaceuticals, a company co-founded by Thompson, is now testing a drug that treats cases of acute myelogenous leukemia that have been resistant to other therapies by inhibiting the mutated versions of the metabolic enzyme IDH 2. In clinical trials of the Agios drug, nearly 40 percent of patients who carry these mutations are experiencing at least partial remissions.
Researchers working in a lab run by Peter Pedersen, a professor of biochemistry at Johns Hopkins, discovered that a compound known as 3-bromopyruvate can block energy production in cancer cells and, at least in rats and rabbits, wipe out advanced liver cancer. (Trials of the drug have yet to begin.) At Penn, Dang and his colleagues are now trying to block multiple metabolic pathways at the same time. In mice, this two-pronged approach has been able to shrink some tumors without debilitating side effects. Dang says the hope is not necessarily to find a cure but rather to keep cancer at bay in a “smoldering quiet state,” much as patients treat their hypertension.
Warburg, too, appreciated that a tumor’s dependence upon a steady flow of nutrients might eventually prove to be its fatal weakness. Long after his initial discovery of the Warburg effect, he continued to research the enzymes involved in fermentation and to explore the possibility of blocking the process in cancer cells. The challenge Warburg faced then is the same one that metabolism researchers face today: Cancer is an incredibly persistent foe. Blocking one metabolic pathway has been shown to slow down and even stop tumor growth in some cases, but tumors tend to find another way. “You block glucose, they use glutamine,” Dang says, in reference to another primary fuel used by cancers. “You block glucose and glutamine, they might be able to use fatty acids. We don’t know yet.”
Given Warburg’s own story of historical neglect, it’s fitting that what may turn out to be one of the most promising cancer metabolism drugs has been sitting in plain sight for decades. That drug, metformin, is already widely prescribed to decrease the glucose in the blood of diabetics (76.9 million metformin prescriptions were filled in the United States in 2014). In the years ahead, it’s likely to be used to treat — or at least to prevent — some cancers. Because metformin can influence a number of metabolic pathways, the precise mechanism by which it achieves its anticancer effects remains a source of debate. But the results of numerous epidemiological studies have been striking. Diabetics taking metformin seem to be significantly less likely to develop cancer than diabetics who don’t — and significantly less likely to die from the disease when they do.
Near the end of his life, Warburg grew obsessed with his diet. He believed that most cancer was preventable and thought that chemicals added to food and used in agriculture could cause tumors by interfering with respiration. He stopped eating bread unless it was baked in his own home. He would drink milk only if it came from a special herd of cows, and used a centrifuge at his lab to make his cream and butter.
Warburg’s personal diet is unlikely to become a path to prevention. But the Warburg revival has allowed researchers to develop a hypothesis for how the diets that are linked to our obesity and diabetes epidemics — specifically, sugar-heavy diets that can result in permanently elevated levels of the hormone insulin — may also be driving cells to the Warburg effect and cancer.
The insulin hypothesis can be traced to the research of Lewis Cantley, the director of the Meyer Cancer Center at Weill Cornell Medical College. In the 1980s, Cantley discovered how insulin, which is released by the pancreas and tells cells to take up glucose, influences what happens inside a cell. Cantley now refers to insulin and a closely related hormone, IGF-1 (insulinlike growth factor 1), as “the champion” activators of metabolic proteins linked to cancer. He’s beginning to see evidence, he says, that in some cases, “it really is insulin itself that’s getting the tumor started.” One way to think about the Warburg effect, says Cantley, is as the insulin, or IGF-1, signaling pathway “gone awry — it’s cells behaving as though insulin were telling it to take up glucose all the time and to grow.” Cantley, who avoids eating sugar as much as he can, is currently studying the effects of diet on mice that have the mutations that are commonly found in colorectal and other cancers. He says that the effects of a sugary diet on colorectal, breast and other cancer models “looks very impressive” and “rather scary.”
Elevated insulin is also strongly associated with obesity, which is expected soon to overtake smoking as the leading cause of preventable cancer. Cancers linked to obesity and diabetes have more receptors for insulin and IGF-1, and people with defective IGF-1 receptors appear to be nearly immune to cancer. Retrospective studies, which look back at patient histories, suggest that many people who develop colorectal, pancreatic or breast cancer have elevated insulin levels before diagnosis. It’s perhaps not entirely surprising, then, that when researchers want to grow breast-cancer cells in the lab, they add insulin to the tissue culture. When they remove the insulin, the cancer cells die.
“I think there’s no doubt that insulin is pro-cancer,” Watson says, with respect to the link between obesity, diabetes and cancer. “It’s as good a hypothesis as we have now.” Watson takes metformin for cancer prevention; among its many effects, metformin works to lower insulin levels. Not every cancer researcher, however, is convinced of the role of insulin and IGF-1 in cancer. Robert Weinberg, a researcher at M.I.T.’s Whitehead Institute who pioneered the discovery of cancer-causing genes in the ’80s, has remained somewhat cool to certain aspects of the cancer-metabolism revival. Weinberg says that there isn’t yet enough evidence to know whether the levels of insulin and IGF-1 present in obese people are sufficient to trigger the Warburg effect. “It’s a hypothesis,” Weinberg says. “I don’t know if it’s right or wrong.”
During Warburg’s lifetime, insulin’s effects on metabolic pathways were even less well understood. But given his ego, it’s highly unlikely that he would have considered the possibility that anything other than damaged respiration could cause cancer. He died sure that he was right about the disease. Warburg framed a quote from Max Planck and hung it above his desk: “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die.”
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