Red meat gives women strokes? No.

Source: Edmonton Journal

Chris Sturdy emailed me a link to a news article claiming "Eating lots of red meat ups women's stroke risk."   I decided to blog about it because it illustrates the difference between relative and absolute risks, and probable investigator bias or poor study design.  The article states:

"Dr. Susanna Larsson of the Karolinska Institutet in Stockholm and her colleagues looked at 34,670 women 39 to 73 years old. All were free of cardiovascular disease and cancer at the beginning of the study, in 1997."

It goes on:

"During 10 years of follow-up, 1,680 of the women (4 per cent) had a stroke....

"When the researchers divided women into five groups based on how much red meat they reported eating, they found that those in the top fifth, who ate at least 86 grams daily (3 ounces) were at 22 per cent greater risk of cerebral infarction than women in the bottom fifth (less than 36.5 grams, or 1.3 ounces, daily).

"Women who ate the most processed meat (at least 41.3 grams, or 1.5 ounces, a day) were at 24 per cent greater risk of this type of stroke than women who consumed the least (less than 12.1 grams, or less than half an ounce a day)."

From the first sentence in the passage immediately above, we know that in this study, 96% of the women did not have a stroke.  If we go to the abstract of the original study, "Red meat consumption and risk of stroke in Swedish women, we find that the so-called 22% greater risk was calculated on a relative rather than absolute basis.

"During a mean follow-up of 10.4 years, we ascertained 1680 incident cases of stroke, comprising 1310 cerebral infarction, 154 intracerebral hemorrhage, 79 subarachnoid hemorrhage, and 137 unspecified stroke. Total red meat and processed meat consumption was associated with a statistically significant increased risk of cerebral infarction, but not of total stroke, intracerebral hemorrhage, or subarachnoid hemorrhage. The multivariable RR of cerebral infarction for the highest versus the lowest quintile of consumption were 1.22 (95% CI, 1.01–1.46) for red meat and 1.24 (95% CI, 1.04–1.49) for processed meat. Fresh (unprocessed) meat consumption was not associated with total stroke or with any stroke subtype."

 

To clarify, if 4 of every 100 people had a stroke (as in this study), the absolute risk for stroke was 4%.  If in one of the subgroups 5 of every 100 people had a stroke, their absolute risk was 5%.  But if you compare the two groups, the subgroup had a 25% greater risk than the other, because 5% is 25% greater than 4%.  Yet in the one group, 96% of people did not have a stroke, and in the other, 95% did not have a stroke.   

According to the abstract, they recorded 1310 cases of cerebral infarction among the entire population, which means that cerebral infarction occurred in 78% of all stroke cases (i.e. it was the main type of stroke in this population).  Thus, we know that the absolute incidence of cerebral infarction in the low meat group was not more than 4%, and conclude that in the high meat group not more than 5% of subjects had a cerebral infarction type stroke--which means that more than 95% of women eating the so-called high meat diets (more than 3 ounces daily) did not have a stroke.  The absolute difference between the two groups was not more than 1%, but by using relative risk, the authors get to report it as a 22% increase in risk.  Creative accounting.



If you read "Why Most Published Research Findings Are False" you will learn that if a study finds a relative risk difference of less than 100%, the odds are that the findings occurred either by chance, poor study design, or investigator bias.  This study falls in that category, bad science--which is true of almost all epidemiological studies like this.

Now take a close look at the last sentence of the abstract of the journal article:

"Fresh (unprocessed) meat consumption was not associated with total stroke or with any stroke subtype."

What?  In the immediately previous sentence, they stated that red meat was associated with a 22% relative risk in cerebral infarction type stroke, but the last sentence says that fresh meat was not associated with total stroke or any subtype, which would include cerebral infarction.

I feel confused. How can "high" red meat consumption be associated with a 22% greater risk of stroke, and yet not associated at all with total stroke or any stroke subtype?  It seems that the trick must be in combining both fresh and processed red meat to get the positive association.

As you can see from the title of the Reuters report, the first claim got plastered on the headlines, but the last was ignored.   What's up with that?




This study didn't show that eating a diet rich in red meat causes strokes.  On the contrary, it showed that at least 95% of people who eat the so-called high meat diet don't suffer strokes.  It also showed that if you massage the data correctly, you get get a result that will get media attention and support conventional preconceptions.

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Protein Restriction and Longevity: My Initial Impressions

I recently received a copy of Perfect Health Diet by Paul and Shou-Ching Jaminet, in which they suggest limiting protein consumption to promote longevity.  Until I started reading this book, I did not put any effort into reading and evaluating research in this area, although I have had several people point me in that direction.  Reading PHD gave me reason to look into it.  Overall I like the Jaminets' book, so I thought they might be on to something.

The Jaminets cite six scientific papers as support for the idea that protein restriction will promote longevity.  All of these papers report on experiments done with rodents (mice or rats).  I have read five of the papers (I did not read the sixth because it appeared not to be original research) and have some thoughts about them.

The first is “Life-Span Extension in Mice by Preweaning Food Restriction and by Methionine Restriction in Middle Age” by Sun et al.  In this study, after a 7 day control period during which all mice received “standard laboratory chow,” they shifted 51 of the mice to “a diet containing a synthetic mixture of amino acids in lieu of natural sources of protein and including methionine at 0.43% per weight,” and an equal number  were shifted first to “an equivalent diet containing 0.23% methionine by weight and after two further weeks [at the age of 12 months] were shifted to a diet containing 0.15% methionine.”

According to Sun et al:

“The control diet, prepared by Purina Test Diets, Inc. (Richmond, IN), was based upon the AIN-76 formulation. It was compounded using 43% cornstarch, 20% sucrose, 8% corn oil, 5% dextrin, 5% cellulose, 3.6% glutamic acid, vitamin and mineral mix, choline, and a set of defined amino acids in lieu of a protein source.”

The experimental diet was identical in all respects except for the ratio of methionine in the amino acid mix.  In short, this diet contains no whole foods, only refined carbohydrates, amino acids, oils, vitamins, and minerals, and contained a large dose of each sucrose and corn oil rich in omega-6 fatty acids.  Therefore, I find it hard to extrapolate the results to a whole food diet.

Sun et al report the results of this intervention on life span:

“Median longevity was 948 days in the control group (95% confidence interval 884–1,003 days) compared with 1,011 days (95% confidence interval 931–1,085 days) in the Meth-R group, an increase of 7%.”

Thus, we can say that in mice fed a diet of refined nutrients, if after the first third of their lives you switch them to a low methionine diet, they will gain an average of 63 days of life. 

Assuming that you could achieve a similar precision of methionine restriction and the same would happen in humans, a 7% increase in lifespan would add 4.9 years to a base of 70 years, 5.6 years to a base of 80 years, 6 years to a 90 year lifespan, and 7 years to a base of 100 years.  This for enduring two thirds of your life—say, 60 years-- eating a protein- or methionine restricted diet.  I personally don’t find those results compelling enough for me to restrict my protein intake.  I’m gambling a lifetime of restriction for a mere 7 extra years, assuming I don’t die accidentally in the mean time.

The second paper, “Methionine-deficient diet extends mouse lifespan, slows immune and lens aging, alters glucose, T4, IGF-I and insulin levels, and increases hepatocyte MIF levels and stress resistance” by Miller et al.  From the methods portion of this paper, we find that they used the same base diet of purified nutrients used by Sun et al:

“The control diet, prepared by Purina Test Diets, Inc. (Richmond, IN, USA), was based upon the AIN-76 formulation, and contained 0.43% methionine by weight. It was compounded using 43% corn starch, 20% sucrose, 8% corn oil, 5% dextrin, 5% cellulose, 3.6% glutamic acid, vitamin and mineral mix, choline, and a set of defined amino acids in lieu of a protein source. Amino acid concentrations were as follows: 0.93% arginine, 0% cystine, 2.31% glycine, 0.27% histidine, 0.82% isoleucine, 1.11% leucine, 1.15% lysine, 0.43% methionine, 1.16% phenylalanine, 0% tyrosine, 0.82% threonine, 0.18% tryptophan and 0.82% valine. Related diets containing 0.1–0.15% methionine were also prepared by the same company for our use, in which cornstarch was substituted for the diminished methionine; the diet containing 0.15% methionine is available as Catalogue no. 52501 (58MK).”

Miller et al describe their method:

“When the mice were 6 weeks old, half of them were placed on a diet containing 0.43% methionine (‘control’ mice) at age 6 weeks, and the other half were placed on a diet containing lower levels of methionine, initially 0.1%, but then increased at 4 months of age to 0.12% and again at 6 months of age to 0.15% to diminish the incidence of rectal prolapse and early death.” [Italics added]

Wonderful.  They admit here that the diets with restricted methionine apparently increased the incidence of rectal prolapse and early death.  In fact, in the results portion of the paper they state:

“It is clear that the experimental group had a higher risk of death in the first year of the protocol, but that this effect was diminished when methionine levels were raised to 0.15%. Survival at ages beyond 365 days was much higher in mice receiving the Meth-R diet. The log-rank test found the difference between the two groups significant at P = 0.02 when all mice were considered, and at P < 0.0002 when only those surviving more than 365 days were considered.”[Italics added]

So the difference in life span reached the highest significance only when they did the calculations leaving out the mice who died early deaths on the methionine deficient diet.  Miller et al report the results on life span:

“Maximum lifespan of the control mice, estimated as the mean age of the oldest 10% to die (1144 ± 26 days, mean ± SD, n = 4), is significantly less (P < 0.002 by Student's t-test) than the corresponding value for the restricted mice (1261 ± 32 days, a minimum estimate with 5% of the mice still living).”

In this study, the restricted mice lived an average of 117 extra days, which is 10% longer than the unrestricted animals.  Note that they achieved this difference by only considering “the mean age of the oldest 10% to die,” in other words, by factoring out the animals that died early in the methionine deficient group.  That is one way to get the conclusion you want.

Again, assuming this could translate to whole foods and humans, you spend your whole life on a border line deficient diet, hoping to avoid early death or rectal prolapse, so that you can live an extra 7 to 10 years.  You decide if the cost justifies that benefit.

The third study is “Low Methionine Ingestion by Rats Extends Life Span” by Orentriech et al.  In this study, “60 Fischer 344 male rats obtained from Taconic Farms were prefed for 2 wk a nonpurified diet (Ralston Purina, St. Louis, MO) were randomly assigned to one of two groups receiving a purified diet containing either 0.86% or 0.17% L-methionine.”

Like Sun et al, they used AIN-76 formulated food, too unlike natural foods to provide a solid base for generalizing to natural diets.  The results:

“Rats fed low methionine (0.17%) starting at 4-6 wk of age showed greater median (1059 vs. 818 d) and maximum (1252 vs. 1116 d) life spans than those fed 0.86% methionine (Fig. 1).When the methionine concentration of the diet was reduced below 0.12% no rats survived for longer than 1 mo (data not shown).”

So the rats on the methionine-restricted diets lived a median of  241 extra days, and when looking at maximum life spans, 136 extra days.  The abstract states the restricted animals lived 30% longer, a number derived by only considering the median life span of each group, as 241 is 30% of 818.  Considering maximum life spans, the difference was only 12%.

There was a cost to the lifelong methionine restriction leading to a 30% greater lifespan:

“On the other hand, rats fed a 0.17% methionine diet from 42 d of age failed to gain weight throughout their lives (Fig. 2). At the end of 90 d of feeding 0.17% methionine to rats, the reproductive organs (testes, seminal vesicles) were smaller and lung and heart were larger (relative to body size) than in rats fed 0.86% methionine.”[Italics added]

The average body mass of restricted rats was 100g from 42 d of age onward, whereas the unrestricted rats had an average body mass of 400g. The unrestricted animals had a body mass 4 times than of the restricted animals, comparable to wild rats which may achieve body mass of 500 g.  This along with the reduced size of the reproductive organs indicates that the greater life span was achieved by restriction of body growth to juvenile size.

Put in human proportions, if 120-150 pounds is adult size, the restricted rats in this study attained weight comparable to about 30-40 pounds. Assuming this applied in some measure to humans eating natural foods, would you trade attainment of mature body size for a 30% increase in life span?

Because this study restricted the rats’ methionine intake from the age of 42 days on, his does not tell us anything about how methionine restriction will affect the lifespan of an adult beginning methionine restriction later in life after attaining mature stature.  

Further, this study only shows that if you’re using a purified diet to feed rats, they will live 30% longer if you restrict their methionine intake to a level that stops the growth process early in life. It does not compare rats on a low methionine refined food diet to rats on a whole foods, self-selected, species appropriate diet.  I would like to see a study examining the difference in life span between rats eating their natural diet for a lifetime, and rats eating this toxic mixture of refined corn oil, sugar, and corn starch.  I really don’t see how anyone can make conclusions about the effect of whole food proteins on human life spans by doing or reading any of these studies of rats eating refined amino acid mixtures. 

The fourth paper, “Lowered methionine ingestion as responsible for the decrease in rodent mitochondrial oxidative stress in protein and dietary restriction possible implications for humans” by López-Torres and Barja, is not even an original experiment, so I did not take the time to track it down for comment.

The fifth study, “Excess methionine suppresses the methylation cycle and inhibits neural tube closure in mouse embryos” by Dunlevy et al, reports that “exogenous methionine unexpectedly caused frequent NTD in cultured mouse embryos.”  (Thanks to Matt Schoeneberger from S.P.E.E.D.  for assistance getting ahold of this article.)  

From the materials and methods section:

“Random-bred CD1 mice were purchased from Charles River, UK.  Embryos were generated by timed matings, explanted at embryonic day (E) 8.5 and cultured in rat serum as described previously [11,12]. Methionine, ethionine, cycloleucine, folic acid or 5-azacytidine (Sigma–Aldrich) were dissolved in PBS and added to cultures as 1% (v/v) additions. The same volume of PBS alone was added to control groups.”

Thus, in this study they cultured mouse embryos outside of the uterus in a solution that contained isolated methionine, resulting in frequent neural tube defects in the embryos.  At most this study shows that when you culture mouse embryos in rat serum instead of the uterus, with the addition of isolated methionine, you get “unexpected” neural tube defects (NTD).  This may show that isolated methionine is a toxin for mouse embryos growing in rat serum, but doesn’t say anything about the effect of natural foods like meat on embryos of any species growing as nature designed, in utero. 

Outside of a laboratory experiment like this, methionine would reach the embryo by route of the mother consuming methionine-rich whole foods which would contain a full complex of amino acids along with nutrients that reduce the incidence of NTD, such as pyridoxine (vitamin B6), cobalamin (B12), or folate, all of which could modify the outcome. The condition of culturing in rat serum lies so far outside the natural course of mouse development that I don’t understand why anyone would assume that this experiment tells us anything about the effect of natural methionine-rich whole foods on the intrauterine development of any species.

The last study, “The atherogenic effect of excess methionine intake” by Troen et al, reports on their experiment with adding isolated methionine to a standard diet:

“Mice were acclimated on a standard rodent maintenance diet recommended by the American Institute of Nutrition and fed ad libitum for 1 week (AIN-93M) (51). They were then systematically assigned to four groups of similar mean body weights and fed for 10 weeks with control and experimental diets formulated on the basis of Hoffman et al. (15) with vitamin-free, ethanol-precipitated casein and the appropriate vitamin mix (Harlan TEKLAD, Madison, WI). A control group continued eating the control AIN-93M diet. Two diets were formulated to induce hyperhomocysteinemia through combined folate, vitamin B12, and vitamin B6 deficiency with or without methionine enrichment: diet “M+B-,” a methionine-enriched/B vitamin-deficient diet, and diet “B-,” a B vitamin-deficient diet with control levels of methionine. A third, methionine- and B vitamin-enriched diet, “M+B+,” was used to determine the effects of dietary methionine enrichment without hyperhomocysteinemia.”

The base AIN-93M diet consists of, by weight, 47% corn starch, 16% dextin, 14% vitamin-free casein, 10% sucrose, 5% cellulose, 4% soybean oil, and the remainder as isolated vitamins, minerals, L-cystine, and t-butylhydroquinone.  Again, a fully refined nutrient diet, to which they added additional refined, isolated methionine and B-group vitamins for the experimental arms.  Again, I don’t see how this can tell us anything about diets composed of whole foods, which still contain unknown components which may modify the effects of any of the components in these refined diets.

The results of methionine-enrichment included increased atherosclerosis:

“Dietary methionine enrichment significantly increased aortic lesion area beyond the baseline vascular pathology of control mice (Fig. 2). The methionine rich, B vitamin-deficient diet (M+B) resulted in a nearly 2-fold increase in lesion area compared with controls (lesion area was 45,923 ± 2,804 μm2 vs. 24,557 ± 1,712 μm2, respectively, P < 0.05). B vitamin enrichment (M+B+) only partially mitigated this increase despite completely normalizing homocysteine levels (lesion area was 37,936 ± 1,298 μm2, P < 0.05 vs. controls).”

Strictly speaking, this study only tells us that adding isolated methionine to a diet, thereby altering the overall ratio of amino acids, increases atherosclerosis. In short, this study shows us that isolated methionine has a toxic, and that its toxic effect can’t be reduced by ingesting isolated B-vitamins.   So, don’t add isolated methionine to your diet!

This study does not tell us that natural foods rich in methionine have the same effect, because they did not test natural foods. In all these studies, the situation is the same as with T. Colin Campbell’s research using isolated casein, not whole milk products, to promote cancer in laboratory animals.  You can’t draw conclusions about whole foods or diets based on whole foods from experiments done with isolated nutrients.

Just to experiment, for a couple of days Tracy and I reduced our meat intake by half.  I reduced my meat intake from more than a pound daily to just about one-half pound, and,  as the Jaminets suggest, replaced the protein with starchy carbohydrates (potatoes and sweet potatoes).  For both Tracy and I, this resulted in a noticeable decline in mood and a dramatic increase in hunger and intestinal gas, along with a disruption of bowel function.

So I remain unimpressed with the results of these studies, and find in them no reason to believe that making any attempt to deliberately restrict my protein intake by conscious decision will have any significant effect on my longevity.  Which brings me to another point.

One of the benefits I have received from paleo dieting has been a sharpening of my primal, unconscious guidance system.  Basically, the longer I have eaten in a “primal” fashion, the less conscious effort I find myself putting into food selection.  I follow my natural inclination to eat meat, fat, vegetables, fruits, and nuts in amounts determined by appetite rather than reason, and I get rewarded with pleasant moods, smooth digestion, abundant energy, and good health.  Every time I interfere with this by trying to impose on my food selection some guidance from the haughty conscious mind, I have negative results, almost always appearing first in the digestive tract and mood. 

The lesson I take from this is that the conscious mind does not know enough to regulate food intake, and, so long as I eat practically primal foods, I am better off if I leave regulation of food intake to primal wisdom of the body.

Understanding “Cleansing” through the lens of Traditional Herbalism

The digestion system is often the first thing to
address when dealing with chronic disease.

What is the best cleanse or detox?

Walk down the supplement aisle at any health food store and you will be bombarded with detox and “cleansing” products. But what exactly is detox and why would we need to do it?

Treat the Person, not the Disease

As an herbalist I do not diagnose or treat diseases. This method is reserved for professionals in the medical industry. 

What does it mean to treat disease? 

Health care in the medical industry can look like this.... Let’s say you have a rash. You go to your doctor. Your doctor diagnoses you with eczema, prescribes a pill or a cream for eczema and then sends you on your way. This is typically a steroid cream which may temporarily take away the rash with frequent applications. 

This is not the way of a traditional herbalist. I do not diagnose diseases and I do not give treatments for disease. That’s fine by me because herbs often don’t work well when using this simplified treatment methods. There are no “rash” herbs or even “eczema” herbs. 

Herbs are most effective when they are used to address underlying problems and bring balance to a person. They are least effective when they are used to suppress a symptom. When a person comes to me with a rash I don’t ask myself, “how do I stop this rash?” Instead I ask, “What is causing this rash?” 

When someone comes to me with the primary complaint of a rash my first questions maybe directly related to the rash. What color is it? Does it itch? It is moist? dry? When did they first notice it? Does it change in severity? 

However I will certainly have a lot of other questions as well. How is that person’s digestion? Do they have frequent bouts of constipation? Do they often feel bloated? How is their immune system? Do they often get sick? How? How is their general emotional state? Are they frequently happy? Frequently angry? 

At the end of all these questions I begin to form a differential diagnosis (based on Traditional Chinese Medicine or Ayurveda). This enables me to understand WHY this rash is happening. By addressing the underlying reason, we can get rid of the symptoms, in this case, a rash. 

Understanding the perspective of the traditional herbalist will help you to understand cleansing through the lens of traditional herbalism. 

Skin is an important eliminatory pathway. Sometimes rashes indicate another eliminatory organ like the liver or colon isn't functionally optimally. 

So, What is the best cleanse or detox?

When a person comes to me requesting a cleanse my first question to them is what are their goals of the detox. 

Sometimes people have very specific health orientated goals. “I don’t want to be constipated.” “I want to have more energy in the morning.” Some have vague complaints or feel they may have a candida overgrowth. 

Oftentimes people want to cleanse because they feel dirty. Perhaps they don’t always eat healthy food. Perhaps they are concerned about environmental toxins. Perhaps they party a lot on the weekends. 

Whatever the reason, these people want to be CLEAN!

How the body works

A simplistic overview of your body is that it takes in nutrients such as air, food, and water. The absorption of these nutrients results in natural metabolic wastes. This may be carbon dioxide from the lungs, bile from the liver, or uric acid from the kidneys. 

Our bodies are designed to eliminate these metabolic wastes. The main organs of elimination are the lungs, liver, colon, kidneys, and skin. When these organs are in balance the naturally occurring metabolic wastes are successfully removed from your body. 


Our bodies are amazingly well designed to keep us healthy! No magic bullet pill or outside measures can replace the job our various organs and systems are designed to do. 

However these organs can get out of balance because of environmental toxins, the inappropriate intake of nutrients, stress, lack of exercise, poor digestion, etc. 


Herbs and lifestyle choices can be employed to help our normal eliminatory functions. 


In my mind a detox is not something we force on our body because it doesn't know how to work. Instead each person's entire body can be analyzed for health, and if appropriate, herbs, food and lifestyle changes like exercise and deep sleep can help the body do it's job. 

When the systems of elimination are out of balance you may experience 

• chronic pain and inflammation frequent headaches
• fatigue
• water retention
• digestive problems such as diarrhea, constipation, gas, bloating
• problems associated with PMS
• skin blemishes
• frequent illness

The lymphatic system plays an important role in cleaning extracellular space
and supporting immune system function. 

The importance of personalized care

You may have noticed in your life that what works for Aunt Jane or what works for your best friend is not what works for you. Because each of us is unique our path of healing will be unique as well. 

So, What is the best cleanse or detox?

Most modern day cleanses are a way of purging “toxins” from the body. Sometimes this is necessary. Every system of traditional herbalism has a tradition of these therapies whether they be fasting, sweating, enemas or even therapeutic vomiting. However, traditional herbalism applies these methods for specific individuals, not for the general public! 

A more holistic approach to this would be to evaluate the person’s elimination pathways and use therapies to help them work optimally. 

Is this person constipated? Do they have problems breathing? Are their pores closed and they are unable to sweat? Is their metabolic fire running low? 

Once the individual is understood, a customized path towards wellness can be created. 

No ONE Way

There is no one way towards health. Anyone who tells you that EVERYONE needs to do colonics, or everyone needs to drink bentonite clay or everyone one needs to take a cayenne lemon juice fast is simply misguided. 

Most people who come to me interested in a cleanse are people who really won’t benefit from purging their body. Instead, many of these people need to be nourished with healthy foods and a healthy lifestyle, they need their digestive process to be supported, and most importantly they need personalized care to achieve their optimal health. 

A one-size-fits all cleanse or detox does not often accomplish long term optimal health. 

Simplistic view of Individuals

So how do you choose the appropriate path to wellness? The answer to that is as varied as the population! However here is a very simple view of two types of individuals and the different avenues they may take.  

Cold and Deficient

A person who is cold most of the time, has a pale face, frequently wakes up groggy, has loose stools and dry skin needs a warming and building therapy. Fasting, eating raw foods, herbs like dandelion or burdock are poor choices for this type of person and can exacerbate any problems they are having. Instead this person will likely benefit from building and warming therapies. 

Warm and Excessive

On the other hand, someone who has a red face, always feels hot, sweats easily, has a bellowing voice, and gets pounding headaches frequently would most likely need more cooling and drying therapies. 

What is the Best Detox?

Be wary of the seemingly magical panacea of cleanses and detox. Understand that we are all unique and our paths to wellness will also be unique. 

The best “detox” is one that was designed specifically for you. 

Traditional herbalism is not interested in fads or in temporarily purging the body as a quick fix towards health. Instead, my goal is to optimize digestion and strengthen the various systems and organs of elimination to creating lasting vibrant health. 


Our bodies are miraculous and they are designed to keep us strong and healthy. Supporting the body's natural eliminatory functions goes beyond the temporary fix of purging and serves you better in the long term.

Sign up for your own journey towards health! 

You can learn more about my personal consultations here. 

Here are some other alternative views of Detoxing and Cleansing

What is Detoxification by Todd Caldecott 

Myth of the Herbal Detox, by Sean Donahue

Why A Parasite Cleanse Can Make You Worse by Karen Vaughn

Study: Strength Training Improves Flexibility, Equal To Or Better Than Stretching

Conventional wisdom maintains that stretching improves flexibility and that strength training makes people "muscle bound"--i.e. less flexible.   I have known for years through self-experimentation that this is hogwash, and have often maintained that properly performed strength training improves flexibility on par with stretching. 

Yesterday I learned that a pilot study presented at the American College of Sports Medicine’s 57^th Annual Meeting on June 4, 2010 has confirmed my observations.  The report states:

Researchers compared the two techniques’ effect on flexibility of the same muscle/joint complexes in a five-week intervention.
 
“The results suggest that carefully constructed, full-range resistance training regimens can improve flexibility as well as—or perhaps better than—typical static stretching regimens,” said James R. Whitehead, Ed.D., FACSM, presenting author of the study.

Twenty-five college-age volunteers were randomly assigned to groups performing either resistance training or static stretching. A 12-person control group remained inactive. All were pre-tested on hamstring extension, hip flexion and extension, and shoulder extension flexibility, as well as peak torque of quadriceps and hamstring muscles. The resistance training and stretching programs focused on the same muscle-joint complexes over similar movements and ranges. Post-tests measured flexibility and strength.

The results—which may surprise advocates of stretching to improve flexibility—showed no statistically significant advantage of stretching over resistance training. Resistance training, in fact, produced greater improvements in flexibility in some cases, while also improving strength. [Italics added]

Although this was a "preliminary" study, I have no doubt that the larger study planned will have the same outcome.  Properly performed, strength training can give you strength, flexibility, and cardiovascular fitness as well. 

Grain Consumption By Neanderthals

The recent PNAS  publication of "Microfossils in calculus demonstrate consumption of plants and cooked foods in Neanderthal diets" by Amanda Henry, Alison Brooks, and Dolores Piperno
has created some stir in the paleo diet community and of course among paleo diet opponents.  The abstract of this article:

The nature and causes of the disappearance of Neanderthals and their apparent replacement by modern humans are subjects of considerable debate. Many researchers have proposed biologically or technologically mediated dietary differences between the two groups as one of the fundamental causes of Neanderthal disappearance. Some scenarios have focused on the apparent lack of plant foods in Neanderthal diets. Here we report direct evidence for Neanderthal consumption of a variety of plant foods, in the form of phytoliths and starch grains recovered from dental calculus of Neanderthal skeletons from Shanidar Cave, Iraq, and Spy Cave, Belgium. Some of the plants are typical of recent modern human diets, including date palms (Phoenix spp.), legumes, and grass seeds (Triticeae), whereas others are known to be edible but are not heavily used today. Many of the grass seed starches showed damage that is a distinctive marker of cooking. Our results indicate that in both warm eastern Mediterranean and cold northwestern European climates, and across their latitudinal range, Neanderthals made use of the diverse plant foods available in their local environment and transformed them into more easily digestible foodstuffs in part through cooking them, suggesting an overall sophistication in Neanderthal dietary regimes.

It seems that whenever any evidence arises for grain consumption by prehistory hominins in the Upper Paleolithic age, someone asserts or wonders if this constitutes evidence (no matter how slim) that, contrary to the widely accepted paleo principle, humans have adapted to eating grains.  But before I get to that, let me comment on a part of this abstract.

Henry et al imply in this abstract that some people think that the Neanderthals went extinct because of "the apparent lack of plant foods in Neanderthal diets."  The idea that lack of plant foods caused nutritional deficiencies that wiped out the Neanderthals got entertained by a CNN reporter, Samira Said:

Researchers found starch granules from plant grains in their teeth, leading them to believe the early humans did not -- as previously thought -- have an exclusively meat-based diet. It also debunks the theory that Neanderthals became extinct because of dietary deficiencies.

Let's have some fun unraveling the non-sequitors in this passage.  So you find some starch on the teeth of some Neanderthal remains, which shows that those individuals definitely ate some plants.  Now you leap to the conclusion that "early humans did not....have an exclusively meat-based diet."  This is like finding some starch granules on the teeth of some domestic cats fed commercial cat foods, then concluding that earlier wild cats did not have a carnivorous diet.  It is entirely possible that these particular Neanderthals were at that point in time eating some plant foods (out of desperation), while earlier Neanderthals, or Neanderthals in richer ecosystems, ate an almost exclusively meat diet.

By the way, what does Said mean by the phrase "exclusively meat-based diet"?  Strictly speaking, "meat-based" means just that, based on, or composed primarily of, meat.  To wit, a diet that is 80% meat certainly is "meat-based."   It does not mean exclusively meat, any more than "plant-based" means "exclusively plants."  Thus, "exclusively meat-based" means "only based on meat" which means that the "exclusively" is not even redundant, just plain unnecessary.

I really don't know how any anthropologist could seriously entertain the idea that dietary deficiencies due to lack of plant foods would cause the extinction of Neanderthals, who according to unrefuted stable isotope studies were almost exclusively carnivorous and apex predators.  Just for the record, in their report on their isotopic studies, Richard et al  stated that the Neanderthals "occupied the top trophic level, obtaining nearly [italics mine] all of their dietary protein from animal sources." See that "nearly"?  To refresh the memories of Henry et al, "nearly" means "almost."  In other words, from isotopic studies we already knew that Neanderthals ate some plant foods.


Further, previous researchers had already previously established that Neanderthals consumed grass seeds, legumes, and other plant foods, as discussed by Dr. BG in her blog post Neanderthals Consumed Grains and Legumes.  However, these previous researchers also established that "cereal grains were an insignificant food source" for Neanderthals; making me wonder why these three researchers presented their findings as if it established that grains were a mainstay and hedge against nutritional deficiencies for the Neanderthals.  Do they have an axe to grind?
 
Back to those who entertain the idea that dietary deficiencies due to lack of plant foods would cause the extinction of Neanderthals.  Have they no knowledge of the Inuit?  Inuit people clearly show that humans can live indefinitely and reproduce successfully for millenia eating almost nothing but animal products.  How could lack of plant foods kill off a species that obviously can obtain all its nutritional requirements from consumption of the various parts of animals?  Its like believing that the lions could go extinct for lack of salads and goji berries.  It could only happen indirectly i.e. not enough plants for their prey.

Henry et al are referring to Neanderthal remains found in Shanidar cave in Iraq, and Spy, Belgium.

Shanidar Cave.  Source:  Wikipedia

The Shanidar III remains they examined date to 60K to 80K years before present (YBP), and the Spy specimens are dated to about 36K YBP.    This means they lived in the Middle to Upper Paleolithic.

Now for a little prehistory lesson.  Humans have been evolving for more than 2 million years.  Most of that time the Earth maintained an ice age environment. According to Wikipedia:

The current ice age, the Pliocene-Quaternary glaciation, started about 2.58 million years ago during the late Pliocene when the spread of ice sheets in the Northern Hemisphere began. Since then, the world has seen cycles of glaciation with ice sheets advancing and retreating on 40,000- and 100,000-year time scales called glacial periods, glacials or glacial advances, and interglacial periods, interglacials or glacial retreats. The earth is currently in an interglacial, and the last glacial period ended about 10,000 years ago. 

During that 2.6 million years, periods of glacial advance exceeded interglacial periods, which typically lasted only 12K years, although some lasted up to 30K years.  During periods of glacial advance, the cold, dry climate favored the growth of grasses but not other plants; and thus it favored the survival of animals that could eat grass, or animals that could eat grass-eating animals.  Isotopic studies such as I cited above, and discussed here as well, clearly show that humans belong among the latter group.  As reported in "A brief review of the archaeological evidence for Palaeolithic and Neolithic subsistence" published here:

There have only been two studies of Palaeolithic modern humans, Homo sapiens sapiens. A study of the isotope values of humans from the late Upper Palaeolithic (ca 13 000 years old) site of Gough's and Sun Hole Cave in Southern England (Richards et al, 2000a) indicated, again by the ¹⁵N values, that the main source of dietary protein was animal-based, and most likely herbivore flesh. The second study (Richards et al, 2001) was a survey of isotope values of humans from Gravettian and later (approximately 30 000-20 000 years old) Eurasian sites. The ¹³C and ¹⁵N values here indicated high animal protein diets....

Between 50K and 21K years before present (YBP), the earth entered a period of full glaciation, during which the climate became colder and drier.   As reported by Science News, between 50K and 3K YBP, 65% of mammal species weighing over 44kg, together with a smaller proportion of mammals of lesser size, went extinct, and it appears that this climate change played a major role in the extinction of the large mammals previously hunted by humans. 


So far, it is only during the Middle and Upper Paleolithic, that we evidence evidence of both Neanderthal and Cro Magnon humans consuming cereal grains.  Given the isotopic studies cited above and known climatic and faunal changes, I would conclude that this situation reflects humans choosing between starving to death and trying to live on previously unexploited plant foods, not a choice of "more balanced, healthier diet," nor what Henry et al decided in their abstract to call "an overall sophistication in Neanderthal dietary regimes."

That line about made me laugh.  So Henry et al think that if Neanderthal people ate a diet composed almost exclusively of meat, then the Neanderthal diet was not "sophisticated," but since they did, they had a "sophisticated dietary regime."  Its as if they think Neanderthals are more respectable if they did eat plants than if they didn't.  Lions must not be "sophisticated" either since they avoid plants. Who cares about sophistication?  What about adaptation?

Which brings me to my speculation.  Why did Neanderthals go extinct?  Maybe you could connect some dots.  Climate change and the hunting prowess of migrating modern humans, equipped with more sophisticated tools, language, shamans, and domesticated dogs, resulted in rapidly declining stocks of mammals, the primary food source for the Neanderthals.  They were like other carnivores supremely adapted to hunting mammals but apparently unlike the African transplant they did not know how to hunt smaller game or seafoods, and did not adapt to more diverse or plant-based diets.  Cro Magnon proved to have the upper hand on hunting in the same ecosystems as Neanderthals, depleting herds rapidly or before Neanderthals could get their hands on them.  Just as would any other true carnivore, they may have gone extinct for lack of meat, not for lack of plants.

In my view, the starch on their teeth is not a mark of sophistication, but of desperation.

Then Homo sapiens sapiens (my we have a high opinion of our selves) went through the same process.  We think we proved smarter and more adaptable by (sort of) adapting grains to us (by cooking), but Nature always has the last laugh.  We've hung on grains for 10K years, but this proves nothing; 10K years is a blink of the evolutionary eye.  Extinction is more the rule than the exception, and agriculture may yet prove to put the proud one out on his ass.

Unless we come to our primal senses.

P.S.  If you like this post and want to see more like it, please consider making a small donation or a recurring subscription payment using the PayPal buttons in the right hand column.  Fighting fallacies is a full time job I love to do, but I need support to continue doing it.  Also consider sending a link to this post to all of your Facebook and other friends.  

Fiber Choice & Beano: The Perfect Pair!

Tracy just found this ad page in one of those local circulars, and commented "Perfect, buy the Beano to deal with the fiber you can't digest!"

A Practically Primal Perspective on Conventional Beef, Part 1: Hormones

7/13/11 update:  I decided that I don't want to endorse or appear to endorse the use of any meat produced by conventional methods of feeding the livestock grains, primarily corn and soybeans.  Since animals consume 80% of the grain and soy produced by U.S. agriculture, this system drives the ongoing destruction of our topsoil both through crops and through grazing.  Animal food production consumes 87% of all freshwater used in the U.S. each year, and thus is the primary driver of depletion of water reserves.  This system also produces most of the water pollution occurring in the U.S.  Our conventional livestock production system has enormous costs detailed in this article from Cornell University.  Since I have known of these costs for more than 20 years, I feel embarrassed and remorseful that I wrote this series and other articles that endorsed the use of conventional animal products.  I served as part of a system that promotes a completely unsustainable approach to human nutrition. 

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Some people wonder if one can safely eat conventional meat as a part of a practically paleo lifestyle.   Documentary films like Food Inc, along with a plethora of anti-meat, pro-vegetarian literature, have given people the impression that conventional meat products come from inhumane production systems and that conventional meat contains hazardous amounts of hormones, antibiotics, and pesticide residues.  Shall we believe this?  Let’s take a look, starting with hormones.

Hormones

Does conventional meat contain hazardous levels of hormones?  Short answer:  No.  For details, read on.

First, a primal perspective.

I once had a native African explain to me that among her people, they have a taboo against hunting female animals.   This taboo makes a lot of sense for a tribe dependent on hunting.  If you kill a female, you are eliminating a bunch of potential offspring at the same time; while killing a few bulls will have essentially no effect on the fecundity of the herd. 

So hunters would have preferred eating bulls to cows, and in Europe still today some producers  raise bulls.  Similarly, in the U.S. we get most of our beef from steer—neutered bulls—while we save the cows for calving and milk production.  

Bulls and steer differ hormonally.  Bull meat samples tested by Fritsche and Steinhart [1] contained medians of 0.34 mg/kg testosterone and 0.32 mg/kg epitestosterone, while steer meat samples (from unsupplemented steers) contain medians of 0.01 mg/kg testosterone and 0.12 mg/kg epitestosterone.   Bull meat had up to 1.05 mg/kg testosterone.  Thus, bull meat contains a median of 34 times more testosterone and more than twice as much epitestosterone than steer meat; and bull meat might have up to 105 times as much testosterone as a steer.

Their data indicates that at least some of the meat typically eaten by hunter-gatherers would have had  between eight and one hundred times more endogenous steroid hormone—in the form of testosterone— than an untreated modern “organic” steer.  Thus, it would seem that through evolution humans adapted to consumption of meat containing considerably greater levels of steroid hormone than what we find in a modern untreated or “organic” steer meat.

Since testosterone promotes muscle tissue growth, a steer has much less growth potential than a bull.  However, testosterone also makes bulls aggressive and harder to handle, so we can more easily control steers.  Modern husbandry attempts to restore the growth potential without the aggression by substituting for a small amount of the lost testosterone other anabolic but less androgenic steroids, primarily estrogens.

Currently the FDA allows the use of five hormones in cattle for meat production: progesterone, testosterone, estradiol-17β, zeranol, and trenbolone acetate.

The first three are natural hormones, the same as produced by an intact animal.   Zeranol occurs naturally also,  produced by fungi.   It acts as a non-steroidal estrogen agonist, meaning it acts like estrogen. Trenbolone acts as an androgenic steroid that promotes muscle growth.

Does the use of these in raising cattle result in meat or dairy products with unusually high, potentially harmful levels of dietary estrogens or other steroids? 

According to Doyle [2], four studies have found that muscle meat from an untreated steer provides estrodiol in a range of 2.8-14.4 pg/g.  Two other studies found estrodiol at concentrations of 12 pg/g in liver, and 12.6 pg/g in kidney.   Doyle also cites an FAO report finding that meat from implanted steers had 9.7 pg/g estrodiol at 15 days after implantation, and 7.3 pg/g at 61 days after implantation.  In short, the levels of estrodiol in hormone-treated meat falls in the normal range found in meat from untreated cattle.  Doyle comments:

“Estradiol levels in edible tissues of implanted cattle are usually significantly higher than in controls but the increases are small, in the ng/kg range. The greatest increases reported in an FAO report on estradiol residues were 0.002, 0.0065, 0.005, and 0.0084 mg/kg for implanted bulls, steers, heifers, and calves, respectively. These increases are well below the FDA recommended limits listed in the table on p. 2 and well below estradiol concentrations in muscles of pregnant heifers (0.016 to 0.033 mg/kg).”

Similarly, Hartmann, Lacorn, and Stienhart examined the “Natural occurrence of steroid hormones in food.” [3]  Using gas chromatography-mass spectrometry, they measured the levels of twelve steroids occurring in market-sourced meats, milk products, plants, yeast, and alcoholic beverages, including both naturally occurring and residues of additional hormones used in production.  They tested beef (bull, steer, heifer), veal, pork, poultry, eggs, fish, and plants (potatoes, wheat, rice, soybeans, haricots beans, muschrooms, olive oil, safflower oil, and corn oil). 

They found no significant difference in hormone levels between meat from hormone-treated and untreated animals.  In the typical diet, meat, poultry, and eggs proved to supply less hormones than non-paleo milk products :

“Meat does not play a dominant role in the daily intake of steroid hormones. Meat, meat products and fish contribute to the hormone supply according to their proportion in human nutrition (average about one quarter). The main source of estrogens and progesterone are milk products (60-80%). Eggs and vegetable food contribute in the same order of magnitude to the hormone supply as meat does.”

Thus, if you eat a paleo diet, and avoid milk products, you actually would eliminate the greatest dietary source of estrogens, and might reduce your total dietary intake of estrogens by more than 50%.

As for health effects of these hormones in foods, Hartmann et al compared the intake of hormones from diet from all sources to natural human hormone production levels, concluding that the food contents of steroids are insignificant compared to endogenous production [p. 18]:

“These values [amounts provided by diet] are far exceeded by the human steroid production (Table 10). Children, who show the lowest production of steroid hormones, produce about 20 times the amount of progesterone and about 1000 times the amount of testosterone and estrogens that are ingested with food on average per day. It has further to be taken into consideration that about 90% of the ingested hormones are inactivated by the first-pass-effect of the liver.  This leads to the conclusion that no hormonal effects, and as a consequence no tumor promoting effects, can be expected from naturally occurring steroids in food.”

For example, a prepubertal boy, most vulnerable to adverse effects of excess dietary estrogens,  produces about 100 micrograms of estrogen daily.  Beef muscle meat contains less than 0.02 micrograms of estrogens per kilogram.  To get from beef an intake of estrogens equal to just one percent of his endogenous estrogen production, i.e. 1 microgram, he would have to consume 50 kilograms--110 pounds-- of beef in a day!  

According to Doyle [2], the lowest observed effect level of exogenous estrogen is 5 micrograms of estrogens per kilogram of body weight.  Thus, a 40 kg prepubertal boy would have to consume 200 micrograms of estrogens daily to observe an effect.  To get this from conventional hormone-treated beef, he would have to consume 10,000 kg of beef every day.  Clearly he isn't going to get feminized by eating beef.

Opponents of the use of hormones in modern animal husbandry often claim that the use of hormones in production of meat and dairy products causes early puberty, obesity, and cancer in modern industrial nations.

Cornell University has a website discussing these Consumer Concerns About Hormones in Foods:

Can steroid hormones in meat affect the age of puberty for girls?
Early puberty in girls has been found to be associated with a higher risk for breast cancer. Height, weight, diet, exercise, and family history have all been found to influence age of puberty (see BCERF Fact Sheet #08, Childhood Life Events and the Risk of Breast Cancer). Steroid hormones in food were suspected to cause early puberty in girls in some reports. However, exposure to higher than natural levels of steroid hormones through hormone-treated meat or poultry has never been documented. Large epidemiological studies have not been done to see whether or not early puberty in developing girls is associated with having eaten growth hormone-treated foods.

A concern about an increase in cases of girls reaching puberty or menarche early (at age eight or younger) in Puerto Rico, led to an investigation in the early 1980s by the Centers for Disease Control (CDC). Samples of meat and chicken from Puerto Rico were tested for steroid hormone residues. One laboratory found a chicken sample from a local market to have higher than normal level of estrogen. Also, residues of zeranol were reported in the blood of some of the girls who had reached puberty early. However, these results could not be verified by other laboratories. Following CDC's investigation, USDA tested 150 to 200 beef, poultry and milk samples from Puerto Rico in 1985, and found no residues of DES, zeranol or estrogen in these samples.

In another study in Italy, steroid hormone residues in beef and poultry in school meals were suspected as the cause of breast enlargement in very young girls and boys. However, the suspect beef and poultry samples were not available to test for the presence of hormones. Without proof that exposure to higher levels of steroid hormones occurred through food, it is not possible to conclude whether or not eating hormone-treated meat or poultry caused the breast enlargement in these cases.

Can eating meat from hormone-treated animals affect breast cancer risk?
Evidence does not exist to answer this question. The amount of steroid hormone that is eaten through meat of a treated animal is negligible compared to what the human body produces each day. The breast cancer risk of women who eat meat from hormone-treated animals has not been compared with the risk of women who eat meat from untreated animals.

Similarly, we don't have any studies of comparing the prostate cancer risk of men who eat meat from hormone-treated animals to men who eat meat from untreated animals.

In Hyperinsulinemic Diseases of Civilization:  More Than Just Syndrome X, Cordain, Eades, and Eades [4] point out that current evidence actually implicates high carbohydrate intake as the promoter of these hormone-related disorders, because high carbohydrate intake raises insulin levels which increases levels of insulin-like growth factors and increases endogenous production of steroids, by far the main source of steroid exposure, while reducing sex hormone-binding globulins that reduce steroid activity. In the abstract they summarize:

Specifically, hyperinsulinemia elevates serum concentrations of free insulin-like growth factor-1 (IGF-1) and androgens, while simultaneously reducing insulin-like growth factor-binding protein 3 (IGFBP-3) and sex hormone-binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor a, insulin-mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body’s endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues, the clinical course of which may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X. [Italics added]

Using the paleo principle to evaluate this claim, we should expect ill effects of hormones in meat to appear in heavy meat-eating hunter-gatherer groups since they ate meat from intact animals, particularly bulls having 10 times as much testosterone as domesticated animals.

Alas for the hormone hypothesis, hunter-gatherers eating strictly native foods had no obesity, and, so far as we can tell, no cancer. [5]  Further, in The Paleolithic Prescription, S. Boyd Eaton, M.D., Melvin Konner M.D., Ph.D., and Marjorie Shostak present data on reproductive milestones among recent hunter-gatherers.  Among three recent hunter-gatherer tribes (Agta, !Kung, Ache), the average age of menarche (onset of menses) is about 16 years of age, compared to 12.5 years in the U.S. according to Wikipedia.

Since hunter-gatherers eating bull meat on a regular basis and consuming around 50% of energy from meat had none of the problems attributed to hormones in meat, it seems unlikely that hormones in meat can account for cancer or any other hormone-related problem in modern people.

I prefer to see people eat meat from animals not treated with hormones or hormone analogues, but if for budget reasons you choose to eat conventional meat (hormone treated or not) instead of grass fed, I think you don't need to worry that its hormone content will harm you in any way.  You should worry more that by avoiding the meat, you will consume too many carbohydrates that will much more profoundly alter your endocrine system in harmful directions.

But before you get meat from hormone-treated animals, check to see if you can find a supplier for meats from animals raised on typical feeds (corn, soy, etc.) but without added hormones.  In Phoenix, we have at least two markets--Sprouts and Sunflower--that supply meat that comes from such animals.
These markets sell their meats at prices comparable and sometimes lower than what I see at more conventional supermarkets where the meat comes from hormone-treated animals.

We will look at antibiotics and other issues in upcoming posts.

Thanks to Matt Schoeneberger, co-author of S.P.E.E.D. Weight Loss Book, for help accessing one of the articles I used as a reference for this article.  

Notes:

1. Fritsche S and Steinhart H. Differences in natural steroid hormone patterns of beef from bulls and steers.  J. Anim. Sci. 1998. 76:1621–1625.  Full text: jas.fass.org/cgi/reprint/76/6/1621.pdf

2.  Doyle E.  Human Safety of Hormone Implants Used to Promote Growth in Cattle:

A Review of the Scientific Literature.  Food Research Institute, University of Wisconsin

Madison, WI 53706.  Full text:  fri.wisc.edu/docs/pdf/hormone.pdf

3.  Hartmann S, Lacorn M, and Stienhart H. Natural occurrence of steroid hormones in food. Food Chemistry 62(1);7-20 

4.  Cordain L, Eades M, Eades M.  Hyerinsulinemic diseases of civilization: More than just syndrome X.  Comparative Biochemistry and Physiology Part A 136 (2003) 95–112.  PDF available here.

5.  Stefanson, V. Cancer:  Disease of Civilization.