Four Brazil Nuts Once a Month

One of the craziest studies I read all year involved feeding people a single serving of Brazil nuts to see what it would do to the cholesterol levels of healthy volunteers. They gave ten men and women a single meal containing zero, one, four, or eight Brazil nuts, and found that the ingestion of just that single serving almost immediately improved cholesterol levels. LDL, so-called “bad” cholesterol levels in the blood, was significantly lower starting just nine hours after the ingestion of nuts, and by no insignificant amount, nearly 20 points within a day. Even drugs don’t work that fast. It takes statins around four days to have a significant effect.

But that’s not even the crazy part.

The researchers went back and measured their cholesterol five days later, and then 30 days later. Now, keep in mind they weren’t eating Brazil nuts this whole time. They just had that single serving of Brazil nuts a month before and their cholesterol was still down 30 days later. It went down and stayed down, after eating just four nuts… That’s nuts!

And no, the study was not funded by the Brazil nut industry.
Interestingly, four nuts actually seemed to work faster than the eight nuts to lower bad cholesterol and boost good cholesterol. These results suggest that eating just four nuts might be enough to improve the levels of LDL and HDL for up to 30 days, and maybe longer—they didn’t test past 30.

Now normally, when a study comes out in the medical literature showing some too-good-to-be-true result like this, you want to wait to see the results replicated before you change your clinical practice, before you recommend something to your patients, particularly when the study is done on only ten people, and especially when the findings are literally just too incredible to be believed. But when the intervention is cheap, easy, harmless, and healthy—eating four Brazil nuts a month—then, in my opinion, the burden of proof is kind of reversed. I think the reasonable default position is to do it until proven otherwise.

They concluded a single serving was sufficient “without producing liver and kidney toxicity.” What they’re referring to is the high selenium content of Brazil nuts—so high that four eaten every day may actually bump us up against the tolerable daily limit for selenium, but not something we have to worry about if we’re just eating four once a month.

I’d be curious to hear if anyone experiences similar results. Even if the study was just a fluke, Nuts May Help Prevent Death by improving the function of our arteries (Walnuts and Artery Function) and fighting cancer (Which Nut Fights Cancer?) and inflammation (Fighting Inflammation in a Nut Shell).

Even eating nuts every day does not appear to result in expected weight gain (Nuts and Obesity: The Weight of Evidence), so enjoy!

This ‘natural green-tea extract’ diet fad is poison

A popular supplement may be destroying your liver…

More and more reports are popping up in the media about individuals taking products with green-tea extract (like some diet pills) and suffering liver damage or complete liver failure.

You may have heard about the teenage boy a few years ago who experienced liver failure – and nearly needed a liver transplant – after taking concentrated green tea extract to burn fat. His chest, face, and eyes were “almost highlighter yellow,” according to the pediatric resident who treated him.

Hospitals report that dietary supplements like green-tea extract account for about 20% of all drug-related liver diseases.

Read that again… dietary supplements make up 20% of drug-related liver diseases. The use of supplements is on the rise in the U.S. Americans spend more than $30 billion per year on nutritional supplements, according to the Nutritional Business Journal. From 2005 to 2014, the supplement industry has grown 85%.

Despite the size of the industry, the Food and Drug Administration (FDA) doesn’t regulate dietary supplements. So you can’t be sure of their safety.

Green tea contains molecules called catechins. In brewed tea, the catechins are at a safe, diluted level.

However, extracts can contain high concentrations of catechins, which can cause liver damage. The severity of liver damage also worsens when you take green-tea extract on an empty stomach, possibly because the catechins interact with glucose.

So dieters popping these pills while starving themselves are at a much higher risk of liver damage. If you or someone you know is taking green-tea extract, throw it out immediately.

Instead, do what I do… Avoid fad pills and enjoy a cup of brewed green tea instead.

Research shows that drinking five to seven cups of this healthy brew a week provides incredible health benefits.

The only problem is that the flavor is simultaneously strong and subtle. It takes some people a while to get used to it. But I can tell you from personal experience that drinking tea is a relaxing and refreshing activity.

In addition to recharging and balancing the body… the real benefit comes from the health-giving chemicals found in green tea.

Green tea is calorie-free, lowers cholesterol, fights cancer, and keeps immune systems strong. Green tea leaves are processed in a way that preserves many of the nutrients known to provide its health benefits.

One final thought to consider… for best results (both for flavor and health benefits), you should drink green tea freshly brewed after allowing it to steep for three to five minutes.

True green-tea aficionados choose the loose leaves and a tea infuser over the prepackaged kind. The health benefits of loose green tea are much greater, due to the quality of the leaves. However, some great (and more convenient) green teas come in bag form.

Here’s how I take my tea…

I prefer tea bags over loose-leaf tea. One of my favorite brands is Bigelow.
I prefer Japanese sencha and jasmine flavors.
I buy and drink green teas that include other flavors from flowers and plants to moderate the sometimes-strong flavor of the green tea.
In the summer, I cook up a pot of tea and boil cranberries in another pot. Then I combine the liquids in a pitcher in the refrigerator for a delicious and naturally sweet iced tea. Year-round, I use a bit of honey to sweeten my tea.
Also, sipping tea can be the perfect time to sit quietly and meditate… even if for just 10-15 minutes a day. The relaxation response triggered with meditation is great for longevity, and combining it with sipping green tea could be a potent way to fight stress and disease.

UNTESTED TREATMENTS FOR LONGEVITY, AND HOW TO TEST THEM

Tests with human subjects require decades, and are impossible to control, so the gold standard for testing claims for treatments that delay aging is the controlled trial with rodents, usually mice. Each treatment is applied to about 50 mice for their 2-3 year life span, and an equal number of controls is housed in identical circumstances. The total cost for a single experiment can run over $200,000, and what we get for this is two full mortality curves, with and without treatment.

You already know that aging research is the most cost-effective in medical science. Medical costs rise steeply with age, and delaying aging by even a small amount carries enormous benefits in avoided suffering, in lives, and in medical costs. Research on life extension treatments in mice is grotesquely underfunded by any reasonable accounting of costs and benefits.

So there is a backlog of treatments that show promise, but we just don’t know yet whether they work. I’m going to list a dozen of my favorites and then propose a novel scheme for testing them at minimal cost. The proposal is to run a rough screening for important increases in lifespan, using a small number of mice, and later to determine the full mortality curves for only the most promising treatments. Further gains in cost-effectiveness can be realized by testing the treatments 2 or 3 at a time. This leaves a lot of disentangling for the statisticians, but math is cheaper than mice. And there is an important fringe benefit: What we really want to know is how to combine treatments to extend health span longer than is possible with any single treatment. Almost nothing is known about how various life extension treatments interact, and it’s high time we started learning.

Here’s my suggested list

Epitalon/Epithalamin

MitoQ/SkQ

Lapachone

Spermidine

Berberine

Dinh lang (Policias fruticosum)

Pterostilbene

Gynostemma pentaphyllum (sold as “AMPK Activator” by LEF)

NAC

Ashwagandha

Turmeric/curcumin

C60

Where do these ideas come from?

The most creative science is also the highest risk, and for that reason is underfunded in today’s economic environment. There are herbs and roots from traditional Chinese medicine and the Indian Ayurvedic tradition; there are experiments run in small, low-budget labs and experiments from Russian universities that will not be given credence until they are validated in Western labs. The ones I am featuring today are substances that I happen to know about, and the universe of promising treatments could be greatly expanded by any expert in Oriental medicine.
A new database of life span studies has recently been announced, to be hosted atgeroprotectors.org. There is an existing catalog of life span studies in animals atlifespandb.sageweb.org, which seems to be unavailable as I write this.

Epithalon/Epithalamin

Decades ago, Vladimir Anisimov of the Petrov Institute in Leningrad began testing purified extracts from pituitary glands for health and longevity benefits. In a lifetime of research, he has found many promising substances. At the top of the list is an extract from a region of the brain known as the epithalamus. The natural extract is known as Epithalamin. The active ingredient is thought to be a short peptide or micro-protein with just 4 amino acids, which Anisimov named Epithalon. In a series of experiments over the years, Anisimov finds life extension in rodents ranging from a few percent to 30%. Treating 70-year-old humans with the extract, Anisimov reports that their mortality rate is cut in half.

MitoQ/SkQ

This is a molecule akin to CoQ10, attached to a positive charge which causes it to be pulled into mitochondria. I have written about it previously here and here. The molecule was developed as a research tool in the 1970s by Vladimir Skulachev and Russian colleagues, and later was recognized for potential health benefits by Michael Murphey and Robin Smith in New Zealand. Skulachev has tested his product SkQ in mice and claims modest life extension. A New Zealand company began selling their version, called MitoQ last year, based on experiments that show improved wound healing and neuroprotective benefits in mice.

Beta Lapachone

Tomas André introduced me to Lapachone a few weeks ago. His French company has begun to promote the science on a web site, though they do not offer it for sale as yet. It is a tri-cyclic molecule extracted from bark of the Pau d’arco tree in the Amazon rain forest. In preliminary studies, it has shown potential promoting arterial health, as a cancer treatment and modifier of the energy metabolism. Most impressive is one study in which the survival curve of mice treated with beta lapachone seems to improve over caloric restriction.

Spermidine

Autophagy is the name of the cell’s main clean-up process, eliminating accumulated wastes. Spermidine promotes autophagy, and is found in many foods. As an anti-aging agent, it has been championed by Frank Madeo of University of Graz. He reports dramatic life extension in worms and flies, and smaller life increases in life span for rodents.

Berberine

Metformin is a diabetes drug that increases insulin sensitivity and dramatically lowers cancer risk. Mice fed metformin live longer. Berberine is a naturally-occurring polycyclic molecule that reportedly has many of the same benefits. It is extracted from the goldenseal root, which has been used in Native American and other cultures as a natural remedy and has been championed by Jonathan Wright, In some studies, berberine improves on metformin both in its effect on glucose metabolism and in improving the lipid profile in the blood. Like metformin, has anti-inflammatory benefits, but it is not known whether it can slash cancer risk as metformin has been shown to do. Recently, concern has been expressed about increased risk of Alzheimer’s in patients taking metformin, and we don’t know how berberine might do on that score.

Dinh lang (Policias fruticosum)

Dinh lang is the Vietnamese name of a traditional herbal remedy. The Parkinson’s drug sold presently as Selegiline or Eldapril or Emsam began life with the name deprenyl. In the 1960s, it was studied by a Hungarian doctor named Joseph Knoll. In one of Knoll’s studies, dinh lang was combined with deprenyl, with the result that each separately extended life span in mice, and two together synergized so that life extension with both was more than the sum of the two separately. I have not seen other studies of dinh lang, and do not know where it can be purchased, or whether it has a place in traditional Chinese medicine.

Pterostilbene

Pterostilbene is a chemical cousin of resveratrol. Both are naturally-occurring, with trace amounts in grapes, wine, blueberries and other berries. Both are a kind of natural anti-biotic, produced by plants as a self-defense when they are threatened by fungal infection.

In 2003, Resveratrol made a splash in the press after an MIT lab discovered that it activated a class of SIR genes associated with longevity. There were high hopes for resveratrol when it was found to lengthen life span in yeast, worms, fruit flies and fish. Performance in mice, however, was disappointing, with life extension only for obese mice on a high fat diet. Pterostilbene appears to have similar activity to resveratrol, but it is much better absorbed and has greater affinity for its target, so it is used in smaller quantities. Pterostilbene deserves to be tested for life extension potential in rodents.

Gynostemma pentaphyllum

This is the powdered leaf of a traditional Oriental medicinal herb, recently popularized by Life Extension Foundation, which promotes it under the name “AMPK Activator”. In human and rodent studies, it improves insulin sensitivity and lowers blood sugar. In studies with fruit flies, it modestly increases life span, but it has not yet been tested for life span effect in rodents.

N-Acetyl Cysteine

Glutathione is a first-line mitochondrial antioxidant, and it is the only antioxidant for which there is any evidence of life span extension. Unfortunately, we cannot absorb glutathione orally, and NAC has been promoted as the next best thing, as the body uses it to make glutathione. A study from Jackson Lab reports significant life span extension from NAC in male mice, but it comes with a warning about reliability of experimental protocol. Here is a study that reports that NAC can slow the loss of brain cells in aging mice.

Ashwagandha

Withania somnifera is an Indian root herb that is used as a longevity aid in the Ayurvedic tradition, and is reported to have anti-cancer benefits. It is a common ingredient in those herbal mixtures that promote telomerase without astragalosides (Product B, PrimalForce, Telo-100, ProxyStem).

Curcumin

Curcumin is an extract from the curry spice turmeric that has been used in traditional Ayurvedic medicine. It is one of the best herbal anti-inflammatory agents, and has been found to extend life span in flies and worms. Based on epidemiology and cell cultures, a role in preventing Alzheimer’s Disease has been proposed for curcumin.

C60

Buckminsterfullerene is a spherical molecule made of 60 carbon atoms that was hiding in plain sight before being discovered in the 1980s. Based on one spectacular report of life span extension in rats three years ago, it has been adopted by people willing to experiment on themselves, who share their experiences, for example, on the Longecity web site.

Pathways and Interactions

In some cases, we expect combining treatments to be a kind of duplication of effort. It may be that the net benefit of A and B is just A. For example, many of the treatments that are known to extend life span work through the biochemical pathway of insulin sensitivity and the glucose metabolism. There are only a few years of human life available from this pathway, and once we add those years, no amount of tinkering with the insulin pathway will get us any more.

Conversely, if we can indeed address two pathways that are fundamentally different, then we expect positive synergies. It may be that the net benefit of A and B together is greater than A+B.
We have a handful of interventions that reliably extend life span in mice: besides dietary treatments such as caloric restriction, protein restriction and intermittent fasting, there is rapamycin, metformin, aspirin, maybe TA-65, some short peptides and various anti-inflammatories. Very little is known about their interactions, and yet there are humans (some of whom read this column) who are not waiting for the data, but doing all these things at once.

Experimenting with multiple treatments

I think it is important both to gather information about new treatments individually, and to begin collecting information about how they combine and interact when applied together. So I have put together an experimental plan using pairs of treatments. Since the number of pairs is much larger than the number of treatments, I propose using a small number of mice for each treatment. For example, with 12 treatments, there are 66 pairs of treatments. If there are just 5 mice assigned to each pair of treatments, that’s 330 mice in all–a manageable number. This is a modest experimental effort compared to the potential for new information about 12 treatments and their interactions. With just 5 mice for each treatment pair, the statistical power for each combination is low. But there will be 55 mice receiving each one of the 12 treatments, so information is there, and the math can extract it. With so few mice, we will not be able to get the clean survival curves that have become the gold standard for testing treatments in mice. But with a technique called incremental multivariate regression, it is possible to untangle the data and determine which are the most promising treatments, and how they are likely to work in combination.
I have begun to circulate this proposal with people who are best able to implement it, and others who are best able to find funding for the project. In coming weeks, I’ll let you know what happens.

UNTESTED TREATMENTS FOR LONGEVITY, AND HOW TO TEST THEM

Tests with human subjects require decades, and are impossible to control, so the gold standard for testing claims for treatments that delay aging is the controlled trial with rodents, usually mice. Each treatment is applied to about 50 mice for their 2-3 year life span, and an equal number of controls is housed in identical circumstances. The total cost for a single experiment can run over $200,000, and what we get for this is two full mortality curves, with and without treatment.

You already know that aging research is the most cost-effective in medical science. Medical costs rise steeply with age, and delaying aging by even a small amount carries enormous benefits in avoided suffering, in lives, and in medical costs. Research on life extension treatments in mice is grotesquely underfunded by any reasonable accounting of costs and benefits.

So there is a backlog of treatments that show promise, but we just don’t know yet whether they work. I’m going to list a dozen of my favorites and then propose a novel scheme for testing them at minimal cost. The proposal is to run a rough screening for important increases in lifespan, using a small number of mice, and later to determine the full mortality curves for only the most promising treatments. Further gains in cost-effectiveness can be realized by testing the treatments 2 or 3 at a time. This leaves a lot of disentangling for the statisticians, but math is cheaper than mice. And there is an important fringe benefit: What we really want to know is how to combine treatments to extend health span longer than is possible with any single treatment. Almost nothing is known about how various life extension treatments interact, and it’s high time we started learning.

Here’s my suggested list

Epitalon/Epithalamin

MitoQ/SkQ

Lapachone

Spermidine

Berberine

Dinh lang (Policias fruticosum)

Pterostilbene

Gynostemma pentaphyllum (sold as “AMPK Activator” by LEF)

NAC

Ashwagandha

Turmeric/curcumin

C60

Where do these ideas come from?

The most creative science is also the highest risk, and for that reason is underfunded in today’s economic environment. There are herbs and roots from traditional Chinese medicine and the Indian Ayurvedic tradition; there are experiments run in small, low-budget labs and experiments from Russian universities that will not be given credence until they are validated in Western labs. The ones I am featuring today are substances that I happen to know about, and the universe of promising treatments could be greatly expanded by any expert in Oriental medicine.
A new database of life span studies has recently been announced, to be hosted atgeroprotectors.org. There is an existing catalog of life span studies in animals atlifespandb.sageweb.org, which seems to be unavailable as I write this.

Epithalon/Epithalamin

Decades ago, Vladimir Anisimov of the Petrov Institute in Leningrad began testing purified extracts from pituitary glands for health and longevity benefits. In a lifetime of research, he has found many promising substances. At the top of the list is an extract from a region of the brain known as the epithalamus. The natural extract is known as Epithalamin. The active ingredient is thought to be a short peptide or micro-protein with just 4 amino acids, which Anisimov named Epithalon. In a series of experiments over the years, Anisimov finds life extension in rodents ranging from a few percent to 30%. Treating 70-year-old humans with the extract, Anisimov reports that their mortality rate is cut in half.

MitoQ/SkQ

This is a molecule akin to CoQ10, attached to a positive charge which causes it to be pulled into mitochondria. I have written about it previously here and here. The molecule was developed as a research tool in the 1970s by Vladimir Skulachev and Russian colleagues, and later was recognized for potential health benefits by Michael Murphey and Robin Smith in New Zealand. Skulachev has tested his product SkQ in mice and claims modest life extension. A New Zealand company began selling their version, called MitoQ last year, based on experiments that show improved wound healing and neuroprotective benefits in mice.

Beta Lapachone

Tomas André introduced me to Lapachone a few weeks ago. His French company has begun to promote the science on a web site, though they do not offer it for sale as yet. It is a tri-cyclic molecule extracted from bark of the Pau d’arco tree in the Amazon rain forest. In preliminary studies, it has shown potential promoting arterial health, as a cancer treatment and modifier of the energy metabolism. Most impressive is one study in which the survival curve of mice treated with beta lapachone seems to improve over caloric restriction.

Spermidine

Autophagy is the name of the cell’s main clean-up process, eliminating accumulated wastes. Spermidine promotes autophagy, and is found in many foods. As an anti-aging agent, it has been championed by Frank Madeo of University of Graz. He reports dramatic life extension in worms and flies, and smaller life increases in life span for rodents.

Berberine

Metformin is a diabetes drug that increases insulin sensitivity and dramatically lowers cancer risk. Mice fed metformin live longer. Berberine is a naturally-occurring polycyclic molecule that reportedly has many of the same benefits. It is extracted from the goldenseal root, which has been used in Native American and other cultures as a natural remedy and has been championed by Jonathan Wright, In some studies, berberine improves on metformin both in its effect on glucose metabolism and in improving the lipid profile in the blood. Like metformin, has anti-inflammatory benefits, but it is not known whether it can slash cancer risk as metformin has been shown to do. Recently, concern has been expressed about increased risk of Alzheimer’s in patients taking metformin, and we don’t know how berberine might do on that score.

Dinh lang (Policias fruticosum)

Dinh lang is the Vietnamese name of a traditional herbal remedy. The Parkinson’s drug sold presently as Selegiline or Eldapril or Emsam began life with the name deprenyl. In the 1960s, it was studied by a Hungarian doctor named Joseph Knoll. In one of Knoll’s studies, dinh lang was combined with deprenyl, with the result that each separately extended life span in mice, and two together synergized so that life extension with both was more than the sum of the two separately. I have not seen other studies of dinh lang, and do not know where it can be purchased, or whether it has a place in traditional Chinese medicine.

Pterostilbene

Pterostilbene is a chemical cousin of resveratrol. Both are naturally-occurring, with trace amounts in grapes, wine, blueberries and other berries. Both are a kind of natural anti-biotic, produced by plants as a self-defense when they are threatened by fungal infection.

In 2003, Resveratrol made a splash in the press after an MIT lab discovered that it activated a class of SIR genes associated with longevity. There were high hopes for resveratrol when it was found to lengthen life span in yeast, worms, fruit flies and fish. Performance in mice, however, was disappointing, with life extension only for obese mice on a high fat diet. Pterostilbene appears to have similar activity to resveratrol, but it is much better absorbed and has greater affinity for its target, so it is used in smaller quantities. Pterostilbene deserves to be tested for life extension potential in rodents.

Gynostemma pentaphyllum

This is the powdered leaf of a traditional Oriental medicinal herb, recently popularized by Life Extension Foundation, which promotes it under the name “AMPK Activator”. In human and rodent studies, it improves insulin sensitivity and lowers blood sugar. In studies with fruit flies, it modestly increases life span, but it has not yet been tested for life span effect in rodents.

N-Acetyl Cysteine

Glutathione is a first-line mitochondrial antioxidant, and it is the only antioxidant for which there is any evidence of life span extension. Unfortunately, we cannot absorb glutathione orally, and NAC has been promoted as the next best thing, as the body uses it to make glutathione. A study from Jackson Lab reports significant life span extension from NAC in male mice, but it comes with a warning about reliability of experimental protocol. Here is a study that reports that NAC can slow the loss of brain cells in aging mice.

Ashwagandha

Withania somnifera is an Indian root herb that is used as a longevity aid in the Ayurvedic tradition, and is reported to have anti-cancer benefits. It is a common ingredient in those herbal mixtures that promote telomerase without astragalosides (Product B, PrimalForce, Telo-100, ProxyStem).

Curcumin

Curcumin is an extract from the curry spice turmeric that has been used in traditional Ayurvedic medicine. It is one of the best herbal anti-inflammatory agents, and has been found to extend life span in flies and worms. Based on epidemiology and cell cultures, a role in preventing Alzheimer’s Disease has been proposed for curcumin.

C60

Buckminsterfullerene is a spherical molecule made of 60 carbon atoms that was hiding in plain sight before being discovered in the 1980s. Based on one spectacular report of life span extension in rats three years ago, it has been adopted by people willing to experiment on themselves, who share their experiences, for example, on the Longecity web site.

Pathways and Interactions

In some cases, we expect combining treatments to be a kind of duplication of effort. It may be that the net benefit of A and B is just A. For example, many of the treatments that are known to extend life span work through the biochemical pathway of insulin sensitivity and the glucose metabolism. There are only a few years of human life available from this pathway, and once we add those years, no amount of tinkering with the insulin pathway will get us any more.

Conversely, if we can indeed address two pathways that are fundamentally different, then we expect positive synergies. It may be that the net benefit of A and B together is greater than A+B.
We have a handful of interventions that reliably extend life span in mice: besides dietary treatments such as caloric restriction, protein restriction and intermittent fasting, there is rapamycin, metformin, aspirin, maybe TA-65, some short peptides and various anti-inflammatories. Very little is known about their interactions, and yet there are humans (some of whom read this column) who are not waiting for the data, but doing all these things at once.

Experimenting with multiple treatments

I think it is important both to gather information about new treatments individually, and to begin collecting information about how they combine and interact when applied together. So I have put together an experimental plan using pairs of treatments. Since the number of pairs is much larger than the number of treatments, I propose using a small number of mice for each treatment. For example, with 12 treatments, there are 66 pairs of treatments. If there are just 5 mice assigned to each pair of treatments, that’s 330 mice in all–a manageable number. This is a modest experimental effort compared to the potential for new information about 12 treatments and their interactions. With just 5 mice for each treatment pair, the statistical power for each combination is low. But there will be 55 mice receiving each one of the 12 treatments, so information is there, and the math can extract it. With so few mice, we will not be able to get the clean survival curves that have become the gold standard for testing treatments in mice. But with a technique called incremental multivariate regression, it is possible to untangle the data and determine which are the most promising treatments, and how they are likely to work in combination.

I have begun to circulate this proposal with people who are best able to implement it, and others who are best able to find funding for the project. In coming weeks, I’ll let you know what happens.

多方面補健 「乙醯半胱胺酸」（N-Acetyl Cysteine）

這是一個很難回答的問題。人體中有很多個不同種類、不同構造的細胞，各有特殊功能。在身體整體而言，只要一個功能有缺失，健康便會打折扣。

除非有一個補健食品能照顧到所有的細胞，否則「百密一疏」。另一方面，即使有一個補健食品能幫助總數涵蓋達99%的細胞功能，那一個剩餘1%的漏洞，便可以是金庸筆下武功高強者的所謂「罩門」：強如陳玄風，能被小孩郭靖刺死。

坊間有不少「保健食品」，吹噓能「提升免疫力」。有些人照字面解釋：「免疫」者，避免疫症也；愈強則愈能高枕無憂。錯了。

很多疾病的病理機制與免疫無關，例如老人退化症、水囊、肌瘤。還有相反的現象：不少疾病之來由，乃是在於免疫系統的反應太強，例如紅斑狼瘡、牛皮癬、第一型糖尿病、多發性硬化、紅膜炎、類風濕關節炎等。單純地「提升免疫力」，乃是匹夫之勇，可以幫倒忙。

總之，沒有任何東西可以「保」證「健」康，也沒有任何東西可以「保」持「健」康，我們只能想辦法「補」充日常「健」康所需的不足而已。

我曾與（現已故的）百草堂老闆周文軒先生交談。他知道我是從事研究工作的，所學的是免疫學，於是問我：有沒有一個補健食品能「調節」免疫，在它低迷時提升之，在它亢奮時抑制之。

換言之，有沒有一個補健食品既適合（失去抵抗力的）愛滋病人，也適合（免疫力過火而控制它不了的）紅斑狼瘡病人。我答說：沒有；哪會有一本天書或是一個萬靈丹？唯一能做的是，所謂「見招拆招」。

好罷，如果沒有一個「百搭」的補健食品，能有一個「數十搭」甚至「十數搭」或「數搭」的也好；也就是說，要「有多種補健作用的」。

那倒不難找。隨手撿來，有一個叫「乙醯半胱胺酸」（N-Acetyl Cysteine）的補健食品，就正能幫助增強/挽救視力，紓緩糖尿病，中和氧游離基，保護心肌細胞、紅血球、肝細胞，對心、肝、肺、腎、腦、眼、皮膚都有補健作用。下一篇再詳述。

保護視力

有一個可以最終令人失明的遺傳病，叫「視網膜色素病變」（Retinitis Pigmentosa, RP）。患此病者，先是出現夜盲，之後視力退化，以至最後失明。追本溯源，RP病變的前因，是在於「視幹細胞」凋亡。

我們的眼睛中有視網膜；憑其上的細胞，我們能接收到視像的訊息，繼而將訊息傳到腦，於是能「看見」。這些細胞主要包括上述的「視幹細胞」（負責接收彩色影像）和「視錐細胞」（只能分辨黑白）。前者的數目較後者多達約百倍。

RP病人視幹細胞的「遺傳基因」有缺陷，以致視幹細胞在出生後逐漸死亡；這便麻煩了。原來，每一次當有光線投射在視網膜時，光線（中的藍色部分）會刺激「視網膜細胞」內一個叫Lipofuscin的蛋白質，從而衍生一種叫A2E的氧游離基。氧游離基乃是「游離分子」，其化學的組成很不穩定，會到處去侵襲其他物體的電子組成，令後者受傷。「視網膜細胞」可以是其肆虐對象之一。為此之故，視幹細胞和視錐細胞內都有一些「抗氧化物質」，例如「谷胱甘肽」（Glutathione），用以將A2E「中和」，以作保護。但由於RP病人的視幹細胞逐漸凋亡，視錐細胞要肩負「中和」A2E的全責；這樣一來，真的是「鞠躬盡瘁，死而後已」。所以，RP病人最終會有失明之虞。

有一個可以幫助「補」充身體「健」康不足的「補健食品」，叫「乙醯半胱胺酸」（N-Acetyl Cysteine，簡稱NAC），能中和氧游離基，包括A2E（J. Cell Physiol., Vol. 226, pp. 1843-1849），於是服後可保護視錐細胞。

正因為NAC能有效地中和氧游離基，它亦能幫助應付另一個叫青光眼（Glaucoma）的眼疾。每當心臟缺氧，心肌細胞不能從一個叫「氧化磷酸化」（Oxidative Phosphorylation）的機制去製造足夠的能量時，會被迫使用儲存在生物電池（叫「腺苷三磷酸」ATP）內的能量。在過程中如果一直缺乏氧氣供應，山窮水盡，可以去到將能量「榨乾」的地步。之後一旦氧氣供應回復正常（這叫「缺氧/再灌注」Ischemia/Reperfusion），細胞立即「復工」，會產生氧游離基。同樣地，忽高忽低的眼壓，可以令視網膜神經細胞遭遇「缺氧/再灌注」的情況；後者能傷害到視網膜神經細胞而形成青光眼。NAC能消除因「缺氧/再灌注」衍生的游離基，從而保護眼睛（Cell Mol.Neurobiol., Vol. 32, pp. 1275-1285）。

續談乙醯半胱胺酸

氧氣是我們身體的必需品；在細胞而言，好比是食糧。但氧氣的使用中，可帶來「氧游離基」，往往造成傷害。身體本來是有基本能力可應付氧游離基的；但若細胞的遺傳基因出了問題，令細胞無法中和游離基，可以成為病，最終甚至死亡。

「G6PD缺乏症」是例子之一。G6PD的全名叫Glucose-6-Phosphate Dehydrogenase。這是一個紅血球的酵素。紅血球負責攜帶氧氣；氧氣中含有小量的游離基。紅血球是用一些叫「谷胱甘肽」（Glutathione）的「抗氧化物質」，以「中和」這些游離基的；但在過程中，一旦作用飽和了，便不能再繼續。這就要用到G6PD，憑它的協助，「谷胱甘肽」能回復中和游離基的功能。但如果一個人一生出來就有G6PD方面的缺陷，他的紅血球若遇上大量（例如來自吸煙的）氧游離基，便沒有能力即時將其全部化解，於是受傷。過去數天談的「乙醯半胱胺酸」（N-Acetyl Cysteine，簡稱NAC），能協助中和游離基而保護紅血球（Clin. Exp. Med., Vol. 4, pp. 50-55）。

肝細胞也是用谷胱甘肽來中和游離基的。止痛藥Paracetamol會減少肝細胞的谷胱甘肽，令肝酵素上升。NAC對此有補健之功：它能保護肝細胞，降低肝酵素。

香煙能「惹痰」。從機制方面觀察：黏附在肺組織的煙油、會被駐守在肺的免疫巨噬細胞（Macrophage）誤會，以為來了外來的侵略者。於是，巨噬細胞召喚中性細胞（Neutrophil）。後者趕到，對着敵人（煙油）大噴氧游離基，目的是想將敵人殺死。但是，噴出的這些游離基也會令肺的上皮細胞受傷。於是，肺中的杯細胞（Goblet Cell）會分泌「黏蛋白」（Mucin），用以保護肺的上皮細胞。黏蛋白與肺組織分泌的水混合後，會成為痰。吸煙者的杯細胞特別多，目的是製造多一些黏蛋白保護肺；故此痰也特別多；即使戒了煙亦如是，除非將杯細胞消減。在這方面，NAC能減少杯細胞而助一臂之力（Respiration, Vol. 48, pp. 50-57）。

NAC還能「化」痰。稍解釋。上述這個黏蛋白，含有特別多的半胱胺酸（Cysteine），當一條條黏蛋白的半胱胺酸互相「扣」在一起時（化學上稱這種「扣」為「二硫鍵」Disulfide Bond），會出現「一片片」的黏蛋白，於是痰便稠了。NAC能拆開「二硫鍵」，令黏蛋白再次轉為一條條，是為「化痰」。

乙醯半胱胺酸完結篇

過去多天，一直在談「乙醯半胱胺酸」（N-Acetyl Cysteine，簡稱NAC）這個補健食品，原因在於它能多方面為我們的身體「補」充「健」康所需。在此之前，已介紹了它在保護視力、化痰，以及幫助紅血球和肝細胞抵抗氧游離基的功能，今天繼續。

心臟病是目前最致命的病。若心臟功能衰竭，不能將足夠血液送到腦，連帶腦細胞在缺氧下死亡，情況可以更壞。

心臟功能為何會衰竭？主要原因之一，是心臟肥大（Cardiac Hypertrophy）。引發心臟肥大的元兇叫「白介素18」（Interleukin 18，IL-18）；是它令心臟纖維化及心肌細胞肥大（Mol. Med., Vol. 16, pp. 465-470）。

在什麼情況下會有IL-18出現？若一個人太過緊張，其腎上腺素透過「Beta Adrenergic接受體」、會令駐守在心臟的巨噬細胞分泌IL-18（Am. J. Physiol,. Heart Circ. Physiol., Vol. 303, pp. 11282-11296）。當一個人吃得太鹹，鹽會刺激腎分泌腎素（Renin），後者會把肝造出的「血管緊張素原」（Angiotensinogen）轉為「血管緊張素Ⅰ」（AngiotensinⅠ）。之後，肺上皮細胞把「血管緊張素Ⅰ」轉為「血管緊張素Ⅱ」（AngiotensinⅡ）。後者會刺激心臟細胞分泌IL-18（Shock, Vol. 30, pp. 3-10）。糖尿病患者血液內的「晚期糖基化終端物」（Advanced Glycation Endproucts）能刺激駐守心臟的巨噬細胞分泌IL-18（Asian Pac. J. Cancer Prev., Vol. 13, pp. 1365-1370）。還有，引發心肌硬塞的「缺氧/再灌注」情況，也會刺激駐守心臟的巨噬細胞分泌IL-18。

在這些方面，NAC都能助一臂之力。這個補健食品能抑制巨噬細胞，着令其不將IL-18分泌出來（《中華肝臟病雜誌》，Vol. 11, pp. 656-659）。

NAC對腎臟也有補健作用。它能協助將腎石分解（ACTAs Urol. Esp., Vol. 10, pp. 371-372）；防止腎小球炎（Am. J. Physiol. Renal Physiol., Vol.285, pp. F1138-F1140）。NAC又可以防止皮膚出現白斑（Br. J. Dermatol., Vol. 154, pp. 1071-1097）。它對心、肝、肺、腎、腦、眼晴、皮膚都有補健作用，有資格被選入最佳補健食品名列。

小紅莓補健

牛奶中的成分很多。在牛的身體中剛擠出來的奶是不能立即拿來飲的，須先用離心機，將其中的脂肪（牛油）隔出，留下的才是供飲用的牛奶。脂肪本身含有「乳糜」脂肪微粒（Chylomicron）和「超低密度脂肪蛋白」（Very Low Density Lipoprotein，VLDL），兩者的密度十分接近。去到人體中，「乳糜」會被小腸吸收而成脂肪；VLDL則會經過肝加工後也成為脂肪。之後，它們都會被血管壁內皮細胞的「脂蛋白脂肪酶」（Lipoprotein Lipase，LPL）轉為「低密度脂肪蛋白」（Low Density Lipoprotein，LDL）。LDL乃是「壞膽固醇」，對人體害處多過益處。LDL既是因LPL之功造出來，所以，若能抑制LPL的操作，便能減低LDL。這方面有一個來自天然食物的成分，叫「前花青素」（Proanthocyanidins），吃了可以幫助我們身體，將LPL抑制下來（Br. J. Nutr., Vol. 20, pp. 1-10）。哪些食物含有「前花青素」﹖小紅莓Cranberry是其一（Crit. Rev. Food Sci. Nutr., Vol. 42, pp. 301-316）。要買小紅莓並不難。這東西新鮮摘下來時入口很酸，酸得近乎苦澀；但曬乾了造成類似葡萄乾的一粒粒，可以拿來當「口果」（零食）吃；不過，若想吃得足量以求產生功效，自非服用提純物不可。

以補健食品而言，「前花青素」之功大矣哉。它能抑制「胰脂肪酶」（Pancreatic Lipase）減少徵用「三酸甘油酯」（J. Nat. Food, Vol. 74, pp. 119-128），以致令身體減少這方面的吸收（Mol. Nutr. Food Res., Vol. 54, pp. 37-59）。它可以用來對付（引發尿道炎的）大腸桿菌。尿道炎是一種不容易根治的病。本來，尿道內有尿液，排尿時大可將附於尿道的細菌沖走。不過，大腸桿菌另有神通，它表面有很多叫Fimbriae的鈎，將自己鈎在尿道壁。小紅莓的「前花青素」能拆去那些鈎，於是令大腸桿菌無法逗留（J. Urol., Vol. 177, pp. 2357-2360）。小紅莓的「前花青素」還可以降血壓，那是因為這東西能刺激血管壁內皮細胞的「一氧化氮合成酶」（Nitric Oxide Synthase）製造出「一氧化氮」；後者會透過刺激一個叫Guanyl Cyclase的酵素，造出一個能舒張血管壁平滑肌的cyclic GMP。一旦平滑肌舒張了，正像路面擴闊，交通舒暢；血壓也就會下降（Nutr. Metab. Cardiovasc. Dis., Vol. 19, pp. 491-497）；再而紓緩（血壓的）下壓，以及減低心絞痛。還有，「前花青素」亦可以抗癌。目前西醫對付肺癌的兩個主要標靶藥是Iressa（學名：Gefitinib）和Tarceva（學名：Erlotinib），它們的藥效，主要在於能將一些「外皮細胞生長因子接受體」（Epidermal Growth Factor Receptor，EGFR）壓制住，從而令癌細胞的生長受到抑制。原來，「前花青素」也有壓制EGFR的功能（BMC Complement Altern. Med., Vol. 11, pp. 134-137），進而催使「非小細胞肺癌」的癌細胞自滅（Plos One, Vol. 6, pp.e27444-e27447）。