Saturday, November 26, 2011

Study Indicates Prostate Cancer Is Reversible By Diet




According to the National Cancer Institute, each year in the U.S., 240,890 men get diagnosed with prostate cancer, and 33,720 men die from it.

According to the American Cancer Society,

"About 1 man in 6 will be diagnosed with prostate cancer during his lifetime. More than 2 million men in the United States who have been diagnosed with prostate cancer at some point are still alive today.

"Prostate cancer is the second leading cause of cancer death in American men, behind only lung cancer. About 1 man in 36 will die of prostate cancer."


I have a family history of prostate cancer, so I have a personal interest in prevention and remedy for this disease of civilization.

According to some people, whole grains and legumes cause or promote the diseases of civilization, including cancer.

If this disease is caused by eating grains and legumes, then any diet based on grains and legumes should promote cancer.  If you give men living with prostate cancer a diet rich in whole grains and legumes, you should see a promotion of the cancer.

My friend, Gordon Saxe, M.P.H., Ph.D., M.D., professor of medicine at U.C.S.D.,  has actually tested this hypothesis, albeit unintentionally.

Gordon has lead pilot research in which men with diagnosed with prostate cancer were taught to eat a diet consisting of whole grains, legumes, vegetables, fruits, nuts, and seeds, while eliminating animal  products, based on evidence [discussed here] that this dietary pattern may reduce the risk or progression of prostate cancer.

If whole grains and legumes promote prostate cancer then these men should have had an accelerated progression of their cancers.  However, in the first study, over six months, this intervention produced just the opposite effect:  a 100-fold reduction in the rate of rise of their disease, as measured by the rate of change in levels of prostate-specific antigen (PSA).  As stated by Saxe et al:

"The rate of PSA increase decreased in 8 of 10 men, while 3 had a decrease in absolute PSA. Results of the signed rank test indicated a significant decrease in the rate of increase in the intervention period (p = 0.01). Estimated median doubling time increased from 6.5 months (95% confidence interval 3.7 to 10.1) before to 17.7 months (95% confidence interval 7.8 to infinity) after the intervention. Nine of 10 participants in the study had reduction in the rate of rise of their PSA, a marker for progression of disease."
When 9 of 10 people respond in the very same way to an intervention, in this case with a reduction in rate of rise of PSA, this tends to suggest that the effect is no accident and most likely indicates a definite therapeutic effect of the intervention.

In the second study, involving 14 men, Saxe et al produced a similar result.  In this second study they explored the biological mechanisms involved:

"During the first 3 months of the intervention, as both median WHR and body weight declined significantly, the median rate of PSA rise not only declined but became negative, reflecting a slight reduction in absolute PSA and possibly disease regression in patients with absolute reductions. Conversely, during the second 3 months of the intervention, when median body weight increased (though not significantly), median PSA began to rise again, albeit more slowly than during the period prior to Baseline."
This second study suggested that weight-related metabolic changes may have mediated the reduction in rate of PSA increase.  In other words, the intervention resulted in a loss of body fat and concommitant metabolic changes related to reduction of body fatness, including an increase in sex hormone binding globulin, that influence prostate cancer.

"Assuming that the attenuation of PC progression was mediated by weight-related metabolic changes, a question arises as to what aspect of intervention brought about the observed reduction in adiposity. Earlier 53, we described large increases during months 0–3 in intake of whole grains and vegetables, food groups which are fiber and water-rich, very low in fat, and therefore of low energy density. However, intake of these foods declined slightly during months 3–6. Weight loss during the first three months may possibly have resulted from replacing energy-rich foods with energy-poor foods, and the slight increase in body weight during the second three months may have resulted from a small degree of dietary recidivism." 
So this intervention, based on increasing intake of whole grains, legumes, etc., resulted in body fat reduction during the period when the subjects ate the most of these foods, and body weight increased during the period when these subjects ate less of these foods.  This clearly undermines the idea that diets rich in grains and legumes cause two of the major diseases of civilization, i.e. obesity and cancer.

Saxe et al consider the possibility that any diet that induces weight loss may reduce cancer progression.
"A second question that naturally arises regarding the reduction in adiposity is whether it matters, in terms of effects on prostate cancer progression, how it is achieved. One aspect of this question has to do with the preferred dietary strategy for reducing energy intake. Another facet regards whether it is more desirable to increase energy expenditure or decrease intake to achieve this end. Although our study and its findings did not address these issues, they remain important ones that warrant consideration in the planning and design of future behavioral approaches to the management of progressive PC. What can be said is that while both a plant-based diet and a high-protein, low-carbohydrate diet high in foods of animal origin (such as the popular Atkins diet) may both result in weight loss, the former is far more consistent with the dietary cancer prevention guidelines of various agencies (69).54 "
Some people reject those cancer prevention guidelines of various agencies, which emphasize increased consumption of whole plant foods and decreased consumption of animal products, claiming that whole grains and legumes are the true causes of diseases of civilization.   These two studies, among others, weaken that claim. 

So far, the only studies I can find testing the effect of a low-carbohydrate diet on prostate cancer were done with mice, not men.  In this one, researchers from Duke Prostate Center fed mice with prostate cancer either a "Western" diet,  "low-fat high-carbohydrate" diet, or a zero-carbohydrate diet.  The results:

"Fifty-one days after injection [with xenograft tumors], NCKD mice tumor volumes were 33% smaller than Western mice (rank-sum, P = 0.009). There were no differences in tumor volume between low-fat and NCKD mice. Dietary treatment was significantly associated with survival (log-rank, P = 0.006), with the longest survival among the NCKD mice, followed by the low-fat mice."
I don't have access to the full text, but if done in a typical fashion, all diets would have been pellets made from isolated nutrients (e.g. casein, starch, sugar, etc.) so this can't tell us much about what would happen in humans if we compared a whole foods vegan diet (whole grains, legumes, vegetables, fruits, nuts, seeds) to a zero-carbohydrate diet (meat and fat only).  The effects of a casein-based zero-carbohydrate diet on mice might be very different from the effects of a meat-based zero-carbohydrate diet on humans.

In a second study, Masko et al fed mice diets containing 0, 10, or 20 percent carbohydrate and again injected them with prostate cancer cells.  As a 'control' they fed a group of mice a 12% fat diet, but they did not inject cancer cells into these mice--which to me means they weren't much of a control group, because they differed from the others not only in dietary composition but also in absence of tumor injection.

The full text of this study tells us the components of all diets:  corn oil, lard, milk fat, casein, dl-methionine, dextrine, maltodextrine, corn starch, sucrose, and isolated vitamins and minerals. 

In the low-fat arm, 72% of calories came from carbohydrate, and 50% of total calories came from sucrose, which means that about 25% of total calories came from refined fructose.  Meanwhile, in the 10% and 20% carbohydrate arms, all of the carbohydrate was provided in the form of corn starch. 

This makes me wonder again about diet composition in the other Duke University study cited above.  Were those mice on the low fat diet also eating a 50% sucrose/25% fructose diet?  If so, did this rig the study, intentionally or not, so that the low fat group would have more body fat and shorter lifespan than the zero-carbohydrate group? 

Moving on, all the mice got all of their protein from casein-plus-methionine, none ate any meat.  Most people eating low carbohydrate diets eat cooked meats, not isolated casein, as their main protein source.  Meat is nutritionally complex, and affected by cooking process, in ways that may result in it having a different effect on prostate cancer than casein-plus-methionine.  For example, unlike the casein-methionine mix fed to these mice, meat contains heme iron and if cooked at high heat, heterocyclic amines, all of which have been linked to prostate cancer causation or promotion [e.g. Sinha et al full text].  So it is not clear how a study of mice eating a low carbohydrate diet wherein casein is the main protein will apply to people eating low carbohydrate diets wherein cooked meat, poultry, and fish are the main protein sources.

Masko et al found that the survival rates of the mice in the 0, 10, and 20 percent carbohydrate groups were similar.  They liked this finding because, as they say, people find it extremely difficult to follow zero-carbohdyrate diets, so now they are ready to test the 20 percent carbohydrate diet on human prostate cancer patients. 

Masko et al also found that the mice in the 20% carbohydrate group had the lowest insulin level, about which they comment:

"It was unexpected that the lowest levels of insulin were observed in mice fed with 20% carbohydrate, but there are possible explanations for this phenomenon. First, there is always the possibility for a type I error in the analysis. Second, it is known that low-carbohydrate diets promote insulin sensitivity in animals (38) and humans (39, 40). Thus, it is possible that a diet containing a small amount of carbohydrates may actually improve insulin sensitivity compared with a diet completely lacking of carbohydrates."
Perhaps unknown to Masko et al, it is also 'possible' that a diet containing an even large amount of carbohydrate may actually improve insulin sensitivity compared to a diet with only 20% carbohydrate. In 1971, Brunzell et al [abstract only] evaluated the effect of increased dietary carbohydrate at the expense of fat in humans, both non-diabetic and mildly diabetic.  In the New England Journal of Medicine they reported that after feeding these subjects a diet providing 85 percent of energy as carbohydrate for 10 days,

"Fasting plasma glucose levels fell in all subjects and oral glucose tolerance (0 to 120-minute area) significantly improved ..... Fasting insulin levels also were lower on the high carbohydrate diet; however, insulin responses to oral glucose did not significantly change. These data suggest that the high carbohydrate diet increased the sensitivity of peripheral tissues to insulin."
 An diet supplying 85 percent of energy as carbohydrate is by necessity very low in fat, so perhaps Brunzell et al could have emphasized that this very low fat diet increased insulin sensitivity.  The mice of Masko et al that got the 20 percent carbohydrate diet had a lower fat intake than the mice on the zero-carbohydrate diet; rather than increasing carbohydrate being responsible for promoting insulin sensitivity, perhaps it is reducing fat (replacing it with starch) that does the trick. 

Anyway, the Masko et al study has a few features that make me skeptical that they will have similar results in humans.  I feel curious to see if their approach will have results as good as those found by Saxe et al.

Thursday, November 17, 2011

Twenty-one Day "Daniel Fast" Reduces Insulin Levels by 23%

Also improves multiple metabolic markers

The Biblical book of Daniel includes a description of what some assert to be the first dietary clinical trial recorded in "Western" literature.  In Daniel 1:8-16 (NIV) we find:

"But Daniel resolved not to defile himself with the royal food and wine, and he asked the chief official for permission not to defile himself this way. Now God had caused the official to show favor and sympathy to Daniel, but the official told Daniel, 'I am afraid of my lord the king, who has assigned your food and drink. Why should he see you looking worse than the other young men your age? The king would then have my head because of you.' Daniel then said to the guard whom the chief official had appointed over Daniel, Hananiah, Mishael and Azariah, 'Please test your servants for ten days: Give us nothing but vegetables to eat and water to drink. Then compare our appearance with that of the young men who eat the royal food, and treat your servants in accordance with what you see.' So he agreed to this and tested them for ten days. At the end of the ten days they looked healthier and better nourished than any of the young men who ate the royal food.  So the guard took away their choice food and the wine they were to drink and gave them vegetables instead. "
Daniel 10:2-3 provides a similar passage:
"At that time I, Daniel, mourned for three weeks. I ate no choice food; no meat or wine touched my lips; and I used no lotions at all until the three weeks were over." 
I wonder if these passages might provide some cognitive dissonance for Judeao-Christian followers of low-carbohydrate diets, at least those who take the Bible as guidance from God.

Whether your consider these passages history or fiction, it seems likely to me that the author(s) had some experience that informed it.  The author(s) evidently believed that 'royal food' including meat and wine pollutes and corrupts humans, and that a 10-21 day diet consisting exclusively of "vegetables" would make a person look "healthier and better nourished" than a royal diet, although at that time the meat would have come from grass-finished animals and the wine from 'organically grown' fruits.

Susan Gregory has written a book about the Daniel Fast, so-called because the follower abstains from animal foods and alcohol, while having ad libitum intake of unrefined plant foods.  The book apparently focuses on the 'fast' as a religious, not health care, method.   I myself would not call a eating plan that allows you to eat unlimited plant foods a 'fast.'  To me, doing so sort of implies that you believe that only animal products, not plants, qualify as food.  So I prefer to call this the Daniel Diet.

However, Bloomer et al decided to find out how 21 days on the Daniel Diet affects human health.

They enrolled 43 subjects ranging in age from 20 to 62, six of whom reported adhering to a 'vegetarian' diet before doing the 'fast.'  Bloomer et al give more details:

"Forty-four subjects (13 men; 31 women) were initially recruited to participate and were enrolled in this study. The mean age of subjects was 35 ± 1 years, with a range of 20-62 years. One female subject had a diagnosis of well-controlled type II diabetes (and used oral hypoglycemic agents), and one male subject had a history of coronary artery bypass graft surgery (and used both a statin and Plavix®). Three subjects were hypertensive upon enrollment (BP≥140/90 mmHg; 2 men and 1woman) and seven had hypercholesterolemia (total cholesterol > 200 mg·dL-1; 1 man and 6 women). One man used a beta blocker and one man used an anti-depressant. Three women used anti-depressants, six used oral contraceptives, two used estrogen replacement, two used a sleep aid, one used a statin, and one used an angiotensin II receptor antagonist."
Bloomer et al describe the 'fast' here:
"A Daniel Fast involves ad libitum intake of specific foods, but the food choices are restricted to essentially fruits, vegetables, whole grains, nuts, seeds, and oil. This plan resembles a vegan diet, which has been reported to yield health enhancing properties [16,17]. However, a Daniel Fast is more stringent, in that aside from the exclusion of all animal products, there are no processed foods, white flour products, preservatives, additives, sweeteners, flavorings, caffeine, or alcohol allowed in this plan."
Apparently the subjects liked the intervention:

"Subjects noted that they enjoyed the ad libitum nature of the plan, as well as the wide variety of food choices. In fact, most subjects reported that they would continue implementing many components of the plan into their previous diets."

The following table shows the dietary data of the subjects during the final 7 days of the Daniel 'fast.'

Some notes on the nutritional profile of the 'fast':
  • Total protein intake declined by about one-third, but the average remained at the level recommended for a lean 77 kg/171 pound man.
  • Total carbohydrate intake declined by only about 20 g per day, but as a percentage of calories, total carbohydrate intake increased from 53% to 62%.
  • Fiber intake increased by more than 50% (up 14 g per day)
  • Fat intake declined by 20 g per day, and from 30% of energy to 27% of energy
  • Saturated fat intake declined from 24 g per day to 9 g per day, a reduction of 63%.
  • Polyunsaturated fat intake increased by only 1 g.
  • Omega 3 intake increased by 87 mg (12%) daily.
  • Vitamin C intake increased by about 50 mg daily, but remained at only about 120 mg daily, indicating a rather low intake of vegetables and fruits by my standards.  A produce-dominated diet can easily supply 400+ mg of vitamin C daily, so this diet probably was dominated by grains, legumes, nuts, and seeds low in vitamin C.
  • Vitamin E intake increased by almost 50%.

 The following three tables show some of the changes that occurred over 21 days on the Daniel Fast:

Notable improvements in table 1 include decreases in heart rate, blood pressure, body weight, and body fat.  This study did not find a marked average decline in body weight and body fat mass primarily because almost half (21) of the subjects were classified as normal weight at the outset of the study; these lean people didn't lose weight, so they diluted the weight loss average.  

Fat free mass declined by an average of 1.7 kg, which could have been water or muscle; we can't determine which from this data in table 1 alone.  However, since blood pressure and insulin levels (data below) dropped significantly, I would expect that this lean mass loss consisted primarily of a significant loss of sodium and water in the 10 overweight and 13 obese subjects in the study (because insulin increases sodium retention, hence water retention and blood pressure).

The subjects did report a small decline in mental health.  According to Bloomer et al, "Through completion of a post fast questionnaire, subjects reported that the main enervation of their mental health was the omission of caffeine."  In other words, they had caffeine withdrawal syndrome.


Notable improvements listed in table 3 include:
  • Reduced blood sugar
  • Reduce Blood Urea Nitrogen
  • Slightly reduced AST and ALT, possibly indicating healthier liver function
 Notable improvements:

  • Total cholesterol declined about 30 points to less than 150 mg/dL, a level thought to confer virtual immunity to heart attack and found by Esselstyn to allow reversal of atherosclerosis.
  • Triglycerides declined by about 12%.
  • LDL-C declined to about 76 mg/dL, a level found in wild animals, hunter-gatherers, and newborn infants.
In addition:

"Insulin (pre: 4.42 ± 0.52 vs. post: 3.37 ± 0.35 μU·mL-1; p = 0.10), HOMA-IR (pre: 0.97 ± 0.13 vs. post: 0.72 ± 0.08; p = 0.10), and CRP (pre: 3.15 ± 0.91 vs. post: 1.60 ± 0.42 mg·L-1; p = 0.13) were lowered in a clinically meaningful manner, although this decline failed to reach statistical significance."
This whole foods diet rich in carbohydrates produced a 23% decline in insulin levels, a 26% decline in insulin resistance (measured by HOMA-IR),  and a 49% decline in C-reactive protein, indicating a substantial decline in inflammation.  Although not statistically significant, these are clinically very significant reductions boding well for these subjects.

Did the Daniel Diet affect obese people differently from lean?  Apparently not.

"Although our intention with this study was not to make comparisons between normal weight and overweight/obese subjects, in an attempt to clarify our findings we also analyzed data using a 2 (weight status: normal weight vs. overweight/obese) × 2 (pre/post fast) analysis of variance. No interaction effects were noted for any variable (p > 0.05), indicating that normal weight and overweight/obese subjects respond to the Daniel Fast in a similar manner."
Although not inspired by the Bible, Tracy and I have been eating mostly (well more than 99%) plant foods for a couple of months now, as an ongoing experiment.  We differ from the Daniel Fast in that we have emphasized eating more like a wild chimp or gorilla: lots of green leaves, non-green vegetables (including starchy vegetables), fruits, beans, nuts, and seeds, while limiting whole grains, not including them every day or in large amounts. 

Compared to my previous experiments with diets containing minimal or no animal products, I have recently focused on eating larger amounts of green and starchy vegetables, nuts, and seeds, with limited amounts of beans, even more limited whole grains.  In those past experiments I ate very limited amounts of nuts and seeds but large amounts (2-3 times daily) of whole grains including substantial amounts of home-made whole wheat breads (both sourdough and yeasted) on most days. Now I have many days with no grains at all, and very little wheat in comparison.

We have so far responded very favorably to this produce-dominated, 99%+ plant food approach.  We'll see how it progresses.

Saturday, November 5, 2011

Pharmaceutical Antibiotics Probably Promote Obesity

We may add obesity to the long list of iatrogenic (medicine-caused) disorders.

Katie Moisse of ABCnews online reports that antibiotics may promote obesity.

Her article refers to research done by Dr. Martin Blaser of New York University Langone Medical Center.  Blaser studies the effects of antibiotics on Helicobacter pylori — a bacterium that lives quietly in most but leads to ulcers in some.

In his animal research, Dr. Blaser found that:

"...antibiotics for H. pylori trick the body into eating more by disrupting hunger hormone levels. Indeed, mice given antibiotics get fatter than their untreated counterparts despite having the same diet."
Blaser published his concerns in an editorial in the August 24, 2011 issue of Nature under the title "Antibiotic overuse: Stop the killing of beneficial bacteria."  

I don't have access to that full text article, but in April of this year a team including Blaser published the results of a human intervention study in which they tested their hypothesis that altering intestinal flora with antibiotics influences appetite-regulating hormones and body mass: The effect of H. pylori eradication on meal-associated changes in plasma ghrelin and leptin (full text).


They found that people treated with antibiotics had a 6-fold increase in post-meal ghrelin, a 20 percent increase in leptin levels, and a 5 percent increase in body mass index 18 months after completing the course of antibiotics. 

 Science Daily reports that ghrelin "not only stimulates the brain giving rise to an increase in appetite, but also favours the accumulation of lipids in visceral fatty tissue." [1]  So antibiotics promote central abdominal obesity, the type associated with metabolic syndrome and increasing the risk of diabetes.

Even if this treatment had spectacular success in treating the main complaints of the patients involved, they might not appreciate the side effect of increased obesity.  But it gets worse.  The text contains this passage:


"At baseline, the 38 H. pylori-negative and 44 H. pylori-positive subjects did not differ significantly in median pain, non-pain, and satisfaction scores (data not shown). Among the 21 patients from whom H. pylori was eradicated, there were no significant differences between baseline and follow-up pain scores [Median (IQR) 9 (2-23) vs. 6 (2-15); p = 0.86], non-pain scores [13 (12-16) vs. 10 (10-18); p = 0.28], or satisfaction scores [13 (10-23) vs. 19 (12-20); p = 0.29]. Thus, the observed increase in BMI following eradication (Figure3) was not correlated with diminished dyspepsia that could increase appetite."  [Emphasis added]
According to these authors, pain levels did not differ between people who were H. pylori positive and those who were H. pylori negative.  This might suggest to some people (like myself) that H. pylori does not cause of the problem.  Further, treatment to eradicate H. pylori did not result in any significant reduction in dyspepsia (stomach discomfort).  This again suggests that H. pylori does not cause the problems experienced by the patients.

So, the destruction of H. pylori didn't give the patients significant relief from their main complaint (stomach discomfort), but it did make them fatter.  How do you like that for an effective treatment strategy? 

I hypothesize that the gut flora reflect the diet, and that imbalanced nutrition causes both H. pylori overgrowth and dyspepsia.   If you change the food flowing through the gut, you will change the flora.  Overgrowth of H. pylori only serves as a marker for a particular type of diet, and does not the cause the dyspepsia.  Killing off H. pylori doesn't give people relief from their gut complaints because their gut complaints arise from dietary and stress factors that remain unchanged by eradication of H. pylori.  

How about holiday weight gain?  Many people report gaining weight over the winter, which may coincide with increased (misguided) use of antibiotics for upper respiratory infections.

Not Just Obesity?

According to another article on ABC News online by Mikaela Conley,  "Blaser hypothesized that the overuse of antibiotics may even be fueling the 'dramatic increase' in many illnesses, including type 1 diabetes, allergies and inflammatory bowel disease by destroying the body's friendly flora, or protective bacteria" in his Nature editorial.

Some cancers appear related to antibiotic use as well.

Tamim et al reported finding a dose-response relationship between antibiotic exposure and breast cancer in Canada, with the highest antibiotic exposure linked to a nearly doubled risk of breast cancer:

"The incidence of breast cancer was higher in subjects who had more antibiotic prescriptions during the 1-15 years prior to the index date (RRs = 1.50, 1.63, 1.71 and 1.79 for the four quartiles, respectively, p-trend = 0.0001). Similar results were found when a number of units were considered. We did not find any effect of the timing of antibiotic exposure on breast cancer risk. Similar patterns of increased risk of breast cancer were detected for the specific antibiotic classes."
Tamim et al also reported a dose-response relationship between antibiotic exposure and prostate cancer in Canada, with the highest exposure linked to an almost tripled risk of prostate cancer:
"Antibiotics exposure (number of prescriptions) during the period of 1-15 years in the past was significantly associated with an increased risk of prostate cancer; RR = 1.69, 2.61, 2.71, and 2.83 for the 4 quartiles, respectively, p-trend = 0.0001. When number of units was taken as the exposure definition, similar results were found. We did not find any effect of the timing or class of antibiotic exposure on prostate cancer risk. We found a dose-dependent association between antibiotics exposure up to 15 years in the past and risk of prostate cancer. However, the lack of temporal trends and the absence of class specific effects suggest a noncausal relationship."
Both of these studies suggested a noncausal relationship between antibiotics and cancer.  Since the relationship seems fairly strong on a statistical basis, I would guess that people who use antibiotics often have cancer-promoting lifestyles, whereas those who avoid antibiotic use have cancer-preventive lifestyles.  The habits that make people prone to infections also make them prone to cancers.

Prevalence of Antibiotic Abuse

Conventional physicians most commonly prescribe antibiotics for upper respiratory, sinus, or ear infections, despite the fact that most of these events involve viruses or fungi (sinuses), which are not susceptible to antibiotics. 


Apparently, according to Blaser, the average American child will receive 10 to 20 courses of antibiotics by the time he is 18 years old, and one-third to one-half of pregnant women will receive them during pregnancy. 

This means that the average American probably has disrupted gut flora and increased ghrelin levels before reaching adulthood.

The Herbal Alternative

I haven't used antibiotics for 30 years. 

If I, Tracy, or one of my patients needs help with an acute respiratory illness, I use acupuncture and herbal remedies.  Often the early application of the appropriate herbal formula can reduce the duration of a 'cold' or 'flu' to 3 days or less, compared to the 7 to 10 days typical for these challenges.

For my patients with chronic stomach discomfort associated with ulcers (or not), I use diet changes and if necessary, herbal medicines, with good results.

Evolutionary biology supports the use of herbal antimicrobials.  Plants need to defend themselves against viruses, bacteria, and fungi without pharmaceutical aid.  Natural selection favored the survival of plants that could fend off microbes, so those plants that could produce antimicrobial compounds survived evolution and those that could not, did not.

Plenty of scientific research shows various herbs have strong antimicrobial activities.  For example, following traditional Chinese medical practice, I use formulas containing forsythia fruit to treat sore throats and acne.  Qu et al reported on the antibiotic properties of forsythia components:

"Forsythiaside was found to possess strong antioxidant and antibacterial activity but forsythin was much weaker. Owing to these properties, the study can be further extended to exploit the possible application of forsythiaside as an alternative antioxidant and antibacterial agent of natural origin."
The "possible application"? Physicians trained in Chinese medicine have been using this herb for centuries!

Notice their reductionistic approach based on their limited knowledge.  They believe that forsythiaside is 'stronger' than forsythin because the former performed better in their test than the latter. 


This reflects the pharmaceutical approach, which so far focuses on taking one agent, isolating it and increasing the dose, hoping to find some dose of that one compound that will take down all of the cells in the microbial colony.  This ignores the variability of individual microbes which almost guarantees that no one compound will kill all individual microbial cells in a colony.


Its like thinking that 100 highly amplified violins will produce the same music (have the same effect) as a 100-piece symphony consisting of a dozen different instruments.  Using the example above, people who focus only on one plant compound like forsythiaside because it appears 'strongest' in some laboratory test forget that their test is limited by what they think they know.  They think forsythin is less important because it performed worse on their test. 

But forsythias produce 'weaker' chemicals like forsythin for some purpose, probably unknown to these researchers and to myself.  Not knowing the reason, we can't assume that the 'stronger' compound is the better one in a natural context.

I would wildly guess that in nature, some microbes will survive a huge dose of the 'strong' compound but die on contact with a small dose of the 'weak' compound.

The benefit of whole herbs lies in their provision of multiple antimicrobial compounds, each acting slightly differently from the others, resulting in a whole that exerts a greater effect than any single part--just like a symphony exerts a greater effect than 100 amplified violins.   The multiple angles of defense against microbes provided by a whole herbal extract increases the chance that it will weaken all microbes it contacts, and reduces the opportunity for the microbial colony to develop resistance to any one of the herbal compounds.  

Plants evolved their approach to controlling microbes over millenia.  Do we really think we can by dicking around with our limited intelligence improve on an approach that evolved by a process that we don't and will never understand completely?  

According to my copy of Chinese Medical Herbology and Pharmacology by John Chen PhD, PharmD, OMD, L.Ac., the essential oil of forsythia fruit (Chinese: Lian Qiao):

" ...has demonstrated a broad specturm of inhibitory effects against Staphylococcus aureus, Diplococcus pneumoniae, Bacillus dysenteria, alpha-hemolytic streptococcus, beta-hemolytic streptococcus, Neisseria catarrhalis, Salmonella typhi, E. coli, Mycobacterium tuberculosis, Bacillus proteus, Boretella pertussis, Corynebacterium diphtheriae, leptospira, and some dermatophytes and influenza viruses." (p. 175)
This provides only one example of literally dozens of antimicrobial herbs in the herbal pharmacopiae. 

With this knowledge, I just say no to pharmaceutical antibiotics.

Thursday, November 3, 2011

Fatty Foods and Sugar Addictive Like Cocaine

An article at Bloomberg.com reports:

"Cupcakes may be addictive, just like cocaine.

A growing body of medical research at leading universities and government laboratories suggests that processed foods and sugary drinks made by the likes of PepsiCo Inc. and Kraft Foods Inc. (KFT) aren’t simply unhealthy. They can hijack the brain in ways that resemble addictions to cocaine, nicotine and other drugs.

“The data is so overwhelming the field has to accept it,” said Nora Volkow, director of the National Institute on Drug Abuse. “We are finding tremendous overlap between drugs in the brain and food in the brain.”
"Lab studies have found sugary drinks and fatty foods can produce addictive behavior in animals. Brain scans of obese people and compulsive eaters, meanwhile, reveal disturbances in brain reward circuits similar to those experienced by drug abusers."
To repeat, the director of the National Institute on Drug Abuse believes that  "The data is so overwhelming the field has to accept it."  Read more here.

It seems science has discovered a few new things about how food affects us since the early 20th century when German scientists believed, incorrectly, that insulin made people fat.

Read Stephan Guyenet's series about food reward starting here.

Wednesday, November 2, 2011

Can The Oceans Support Recommended Fish and Fish Oil Intakes?

Like many nutritionists, physicians, and 'public health" organizations, I have previously recommended increased intake of fish and fish oils to raise intake of omega-3 fatty acids, supposed to prevent or remedy cardiovascular and neurological diseases and possibly reduce cancer risk. 

Although the American Heart Association and similar organizations endorse this idea, in 2009 Jenkins et al questioned its wisdom on two bases:  the weakness of evidence for benefits of fish and fish oil intake, and the strength of evidence that global fisheries are collapsing and unable to support current, let alone increased, use of fish and fish oils.
"The main problem with this advice is that, even at current levels of fish consumption, fisheries globally have reached a state of severe crisis (Figure 1).5-8 Already, the demand from affluent and developing economies, particularly newly affluent China, cannot be met by the world's fisheries.6 Moreover, declining catches are increasingly diverted toward affluent markets rather than local ones, with dire consequences for the food security of poorer nations, islands and coastal communities.9"

Uncertain health benefits of fish and fish oil

Jenkins et al  point to a number of problems with the evidence supporting use of fish and fish oils:

1.  Healthy subject effect:  "....fish eaters generally have healthier lifestyles than the rest of the population. They exercise more, smoke less and have better diets.1113"  This makes it very hard to determine whether the better health found among people eating more fish is due to their fish consumption, or to these other habits.

2.  Inconsistent results:  Some interventional studies show benefits from increased intake of fish and fish oils, while others do not, and some, such as DART-2, showed harm, with an increased risk of cardiac death among men who took fish oils.

3.  Vegetarians appear to have a lower risk of cardiovascular disease and death therefrom, despite avoiding fish and fish oils, suggesting that non-fish dietary factors play a larger role.

4.  We have little evidence supporting the use of fish and fish oils for metabolic syndrome, diabetes, or neurological or autoimmune diseases, or even for neurological development. 

Regarding the neurological argument, although Jenkins et al do not mention this, Sanders reviewed the available literature and reported that "There is no evidence of adverse effects on health or cognitive function with lower DHA intake in vegetarians." In addition, Beezhold  et al found a lower incidence of depression among vegetarians than among omnivores, despite lower intake of omega-3 fatty acids among the former.  They reported that "participants with low intakes of EPA, DHA, and AA and high intakes of ALA and LA had better mood," contradicting the hypothesis that depression results from insufficient intake of pre-formed long-chain omega-3 fatty acids. 

Declining Fish Stocks

Jenkins et al report:
"In contrast to the uncertainty over the value of omega-3 fish oils in the scientific literature, there is little doubt about the gravity of the fisheries crisis and the prospect of ongoing collapses of fish stocks. There is scientific consensus about the rapid worldwide decline of fish stocks. Notably, and despite increasing fishing effort, global catches have been in decline since the late 1980s (Figure 1A),5 and the number of collapsed stocks has been increasing exponentially since 1950 (Figure 1B).8,47,48 There are also over 100 confirmed cases of extinctions of marine populations in the world's oceans.49"
"When projected forward, these trends imply the collapse of all commercially exploited stocks by midcentury.7,8 Yet the dire status of fisheries resources is largely unrecognized by the public, who are both encouraged to eat more fish and are misled into believing that we still sail in the sea of plenty.50 Indeed, the species that Westerners are supposed to eat in increasing amounts have stocks that are already under tremendous pressure (e.g., yellowfin tuna, the basis of the much recommended North American “tuna-fish sandwich”51) or that have collapsed, sometimes spectacularly, such as cod off the coast of northeastern Canada.52"

According to an article in the National Geographic, large fish stocks have declined 90 percent since 1950.

On November 2,  2006, Richard Black of the BBC reported on a study published in Science: "There will be virtually nothing left to fish from the seas by the middle of the century if current trends continue."  Black reported:


Steve Palumbi, from Stanford University in California, one of the other scientists on the project, added: "Unless we fundamentally change the way we manage all the ocean species together, as working ecosystems, then this century is the last century of wild seafood."

In short, the drive to eat more fish and fish oils will only accelerate the rate of destruction of marine ecosystems. 

At the very least, our hunger for fish and fish oils will leave future generations with a world wherein they will be unable to eat cod liver oil or fatty fish even if they needed to, because there just won't be any left in the oceans.

Seafood Poisoning

Perhaps people eating increased amounts of seafood will suffer the same fate as ocean fish.  Seafoods commonly contain chemical contaminants that appear to impair fertility, including mercury, PCBs, PEs, and others. 

Rozati et al found, among Indian men:

"PCBs were detected in the seminal plasma of infertile patients but absent in fertile controls (Table 1)."

"...a comparison between fish-eaters and non fish-eaters, irrespective of the dwelling revealed higher PCB concentrations and significantly lower total motile sperm counts in fisheaters than in non fisheaters (Tables 2,3)."
"Fish-eating urban dwellers had the highest PCB concentrations, followed in order by fish-eating rural dwellers, non fish-eating urban dwellers with an exclusively vegetarian diet and non fish-eating rural dwellers with an exclusively vegetarian diet. The total motile sperm counts in these men were inversely related to their PCB concentrations, being the least in fish-eating urban dwellers followed by fish-eating rural dwellers, non fish-eating urban dwellers with an exclusively vegetarian diet and non fish-eating rural dwellers with an exclusively vegetarian diet (Tables 2)."


Another study reported:

“The lowest levels of p,p'-DDT+p,p'-DDE and PCBs were found in milk from lacto-vegetarians and the highest levels in milk from mothers who regularly consumed fatty fish from the Baltic.”
Norén K. Levels of organochlorine contaminants in human milk in relation to the dietary habits of the mothers. Acta Paediatr Scand. 1983 Nov;72(6):811-6.

Does that make fish look like good brain food?