Wednesday, April 18, 2018

Shawn Baker's Carnivore Diet Blood Tests

In an interview with Robb Wolf, Shawn Baker has released some results of his blood tests after more than a year eating only meat and water [transcript]. 

Several vegans, none of whom have any medical education and therefore no competence or business making medical diagnoses, have nevertheless diagnosed Baker as a T2 diabetic because his fasting blood sugar was found to be 127 and his Hb(a)1c was 6.3.   Here's an example:



To start, I would like to point out that these "happy healthy" vegans may have committed a crime in all 50 states:  practicing medicine without a license.  For example, the "happy healthy vegan" who made the video above lives in California.  According to California Penal Code 2052, it is a crime for any person to practice, attempt to practice, or advertise practicing, any treatment of the sick including diagnosis, operation, or prescription for an ailment, blemish, deformity, disease, disfigurement, disorder, injury, or any other physical or mental condition without a valid certificate or authorization for doing so.

Yes, just rendering a biomedical diagnosis is by law considered practice of medicine.  You don't have to offer treatment as well.  I know because I am bound by this law in my profession.

Medical diagnosis is not a simple-minded game of matching blood test results to values given by organizations such as the American Diabetes Association.  If it was then there would be no need to give physicians years of training.  You could practice medicine without any training by just ordering blood tests and then checking to see if any were "out of range' and matched any official guidelines.  Anyone who could read would be able to "practice medicine" if that's all it entailed. 

As expected, having no medical education, this vegan does not understand the concept of differential diagnosis using data from both lab tests and the clinical presentation of the patient.  If he did, he would realize that his diagnosis of Baker is probably unwarranted by the clinical presentation as well as the blood test evidence. 

DIFFERENTIAL DIAGNOSIS

Differential diagnosis is the process a trained physician uses to determine which of various conditions or diseases is the correct diagnosis (explanation) for a particular symptom or sign presented by a patient.   Symptoms, signs and lab values are collected to either confirm or rule out possible diagnoses (explanations) for an individual's presentation.

For example, an man may complain of difficulty urinating (dysuria).   This single symptom occurs in multiple conditions, including: benign prostate hypertrophy, prostate cancer, bladder infection, bladder stones, kidney infections, kidney stones, sexually transmitted diseases, drug side-effects, and lower back pain, to name a few.  Differential diagnosis is the process by which a physician determines which of these conditions most likely accounts for the single symptom in this case.

Pathological fasting high blood sugar (hyperglycemia) can for another example be caused not only by diabetes T2, but also by diabetes T1, certain medications, pancreatitis, pancreatic cancer,  Cushing's syndrome, and some hormone-secreting tumors.

Hyperglycemia also occurs in response to intense glycogen-depeleting exercise and "It could be argued that a hyperglycemic-hyperinsulinemic response after glycogen-depleting exercise creates the appropriate milieu for at least partial restoration of muscle glycogen."  It is well known that the release of catecholamines (e.g. epinephrine, nor-epinephrine) during intense exercise will increase blood sugar levels. 

In intense exercise, these catecholamines increase 14-18 fold to levels seen in pheochromocytoma, an adrenal gland tumor.  This induces a seven- to eightfold increase in glucose production (glucogenesis), which is the largest increase seen under any physiological or pathophysiological condition.  Hence, both intense exercise and the process of recovery from such exercise produce blood levels of substances that would in a sedentary person indicate a probable disease process.

To distinguish the correct diagnosis, the physician must take into account all clinical symptoms and signs, as well as laboratory results if applicable.  Laboratory results are only part of the picture.  One's diagnosis must be consistent with the total clinical picture.

Differential diagnosis is necessary to choose the correct treatment course.  Incorrect diagnosis can lead to rendering a treatment that is at best ineffective, and at worst harmful or even deadly to the patient.

Now let's imagine that Baker actually has pancreatic cancer, but the "happy healthy vegan" was in charge of Baker's treatment.  Since the vegan "knows" that Baker has diabetes, he prescribes a treatment for diabetes.  How would that work out?

This is why non-physicians are warned not to self-diagnose, or to diagnose others. 

NORMAL DOES NOT EQUAL NATURAL, OPTIMAL, OR HEALTHY



Normal blood substance ranges are defined by what is normal – i.e. the norm – in the general population. It is a simple logical fallacy to suggest that what is the norm (normal) is what is desirable or optimal.  If a population is sick, then it is likely that the normal blood values in this population correlate with or represent what happens in a person with underlying disease, not health.

The general population eats a mixed, high carbohydrate diet and has high risks for chronic diseases.  In the present U.S. population, it is normal to be overweight and prediabetic.  Therefore, the normal ranges defined by laboratories probably tell you what levels you will find in normal i.e. sick or borderline sick people who eat a mixed, high carbohydrate diet.

While it is normal (the norm) to be unhealthy, it is presently abnormal to be healthy.  It is even more abnormal to be a world-class athlete who has broken world records and is in the  process of training to break more world records.  Therefore, abnormal blood tests do not necessarily indicate disease, and may in fact indicate health or unique conditions induced by intense physical training of an elite athlete, which are abnormal conditions in the U.S. population. 

Some blood values are responsive to what you eat.  If you dramatically change your  diet, so that you no longer eat a "normal" diet, some of your substance levels will likely no longer be “normal.”  A high protein, high fat, low carbohydrate diet will produce lab values different from a low protein, low fat, high carbohydrate diet.  Since the general population eats a high carbohydrate plant-based diet, anyone who adopts a low carbohydrate, animal-based diet can expect to have abnormal blood values.  That might be a good thing, since, as noted, normal blood values are what we find in the population that normally gets heart disease, diabetes, cancer, dementia, and so on.

Finding abnormal blood values in someone who is displaying excellent health and function is a reason to question whether the normal values are actually desirable in all circumstances.

Shawn Baker is abnormal.  He eats an abnormal diet, and he is a world class athlete engaged in an abnormal amount and intensity of physical activity.  Therefore, I would be surprised if none of his lab values were abnormal. 

INDIVIDUAL VALUES MUST BE INTERPRETED IN CONTEXT

Vegans who have criticized Baker's blood values seem to think that you can diagnose a disease based on one or two lab values. 

As already noted, high fasting blood sugar could indicate several other disease processes, as well as physiological responses to low carbohydrate intake or exhaustive exercise.  To determine which of these fits the Baker case requires critical thinking, problem-solving skills and training in differential diagnosis.

Diabetes mellitus is a disease process, not a lab value, not a glucose level.  The Merck Manual states:  "Diabetes mellitus is indicated by typical symptoms and signs and confirmed by measurement of plasma glucose."  Thus, symptoms and signs are the primary indications; blood glucose measurement is for confirmation. 

Again, according to the Merck Manual, clinical symptoms of diabetes include "glycosuria and thus an osmotic diuresis, leading to urinary frequency, polyuria, and polydipsia that may progress to orthostatic hypotension and dehydration. Severe dehydration causes weakness, fatigue, and mental status changes. Symptoms may come and go as plasma glucose levels fluctuate. Polyphagia may accompany symptoms of hyperglycemia but is not typically a primary patient concern. Hyperglycemia can also cause weight loss, nausea and vomiting, and blurred vision, and it may predispose to bacterial or fungal infections."

Frequent urination, excessive thirst, weakness, fatigue, weight loss...these do not appear to be part of the clinical picture presented by Shawn Baker.  Absence of these symptoms weakens a case for a diagnosis of diabetes.

Regarding T2 diabetes, this is typically characterized by at least two metabolic conditions: high fasting glucose and high fasting insulin, both due to the underlying condition of insulin resistance.  Baker’s insulin level was found very low (2.6; normal range is 2-19.6), indicating high insulin sensitivity.  His triglycerides were also very low (54), consistent with high insulin sensitivity.  This evidence rules against a diagnosis of T2 diabetes.

It also means that Baker's glucose level is not caused by insulin resistance as it is in T2 diabetes.  We have to find another explanation for his glucose levels.

Nor does Baker present a clinical picture warranting a type 1 diabetes diagnosis.  An unmedicated type 1 diabetic would not have enough insulin to maintain Baker’s level of lean mass nor the vitality to be breaking world records in Master’s rowing.

Therefore his blood values probably do not warrant a diagnosis of diabetes nor even borderline diabetes.

Vegans also seem to have ignored Baker's report that his blood sugar drops into the 80s as the day goes on.  In Baker's words: 
"I use to wake up around 115 most days. This day was 127. But what I'll see is that will drop down throughout the day and it'll get down in the afternoon. I'll becoming down into the 80s. And then I'll eat a meal and it may either not go up at all. I've seen it go down afer meals. I've seen it rise at most, maybe ten, 15 points, which again points to very good insulin sensitivity."
Therefore, it seems Baker only has this high blood glucose reading in the morning, but not later in the day nor after meals.  If so, that also rules against a diabetes diagnosis. 

Many people – especially the vegans – evaluating Baker's numbers are very worried about his blood sugar level being high a large part of the day.  I think it is important to note that not-yet diabetic people eating normal diets have increases of blood sugar up to 140 mg/dL after every meal.
"In nondiabetic individuals, plasma glucose concentrations peak ∼60 min after the start of a meal, rarely exceed 140 mg/dl, and return to preprandial levels within 2–3 h."
 Thus, a normal person who eats 3 carbohydrate-rich meals daily has blood sugar levels as high or higher than Baker's for some part of each day, up to several hours.  Thus it is even possible that Baker spends no more or perhaps even less total time with a blood sugar level above 100 than the typical person who eats three carbohydrate-rich meals daily. 

Baker’s unusual fasting blood sugar probably needs another explanation.  To make an educated evaluation of what is going on you need to understand human metabolism and biochemistry, particularly how human metabolism adapts to a very low carbohydrate intake and a high volume of intense, glycogen-depleting exercise.

A likely explanation is: fasting gluconeogenesis.

As I have already noted, it is well established that hyperglycemia also occurs in response to intense glycogen-depeleting exercise and "It could be argued that a hyperglycemic-hyperinsulinemic response after glycogen-depleting exercise creates the appropriate milieu for at least partial restoration of muscle glycogen."  Exercise-induced hyperglycemia is stimulated by catecholamines, which cause hepatic glucose production, evidently to supply working muscles with fuel during exercise, and to replenish glycogen after exercise. 

Glucose production from either amino acids or the glycerol backbone of triglycerides (fats) is called gluconeogenesis.  Muscular athletes who eat little or no dietary carbohydrate but engage in sports demanding glycolysis – such as Baker's sport of rowing, as well as resistance training – depend on their livers to supply blood sugar to the brain, red blood cells, and muscles, via gluconeogenesis.

It is reasonable to postulate that Baker’s liver has upregulated gluconeogenesis to support his brain, blood cells, and very high activity levels in events that require glycogen stores, in the absence of dietary carbohydrate.  His fasting blood sugar is particularly high because after a long fast – required for the blood test – his liver has to be actively generating glucose, but since his insulin level is at a minimum, more of this glucose remains in the blood than in a normal individual who has a higher fasting insulin level.

A doctor named Kraft first identified that 75% of people with “normal” or equivocal glucose tolerance tests had borderline or abnormal insulin response patterns indicating ‘diabetes in-situ’ or ‘occult diabetes.  Later, another team headed by Crofts, and working with Kraft, found that about 75% of people with normal glucose tolerance had hyperinsulinemia.

This leads to the reasonable hypothesis that normal blood sugar levels represent the levels of a population that has some degree of hyperinsulinemia.  In these normal people, a normal elevated insulin level is keeping their glucose level in the normal range.

Since insulin reduces blood sugar levels by stimulating fat cells to extract glucose from blood and convert it to fat, the normal blood sugar level probably also indicates a normal gradual gain of body fat over time.  These normal people may also experience chronic fatigue, because the carbohydrates and fats they are consuming are being preferentially stored via the action of insulin.  

In these normal people the fasting blood sugar level does not rise above 100 until their fat storage capacity is maxed out and their fat cells become insulin-resistant. Then their blood sugar rises to the levels considered to represent diabetes.

A person who eats a high carbohydrate diet might slow down this process by engaging in adequate physical activity, which disposes of excess carbohydrate energy and reduces insulin levels.  However,
a study of blood glucose (BG) levels in athletes consuming high carbohydrate diets (250-450 g per day) found:
"4/10 athletes studied spent more than 70% of the total monitoring time above 6.0 mmol/L [106 mg] even with the 2-hour period after meals is excluded. Fasting BG was also in the ADA defined prediabetes range for 3/10 athletes."
Thirty percent of these athletes had fasting glucose levels that were by ADA standards "prediabetic."  The authors concluded that  "a diet rich in carbohydrates may not be beneficial in some athletes, especially as low BG is unlikely to be of concern to an athlete consuming adequate calorie intake."

Some physically active people, such as Professor Timothy Noakes develop diabetes after years of eating high carbohydrate diets.



In people eating like Baker,  the very low fasting insulin level probably also contributes to a higher fasting glucose.  When fasting insulin is very low,  blood glucose is only very slowly being converted to stored glycogen or body fat, if at all.  Instead that glucose remains in the blood available to fuel the brain, blood cells, and glycolytic activities.  This high glucose availability (due to a low insulin level) may be one reason Baker is an abnormal person, stronger than 99.999% of his peers and capable of breaking world records. 

The point is, we already know that normal people are metabolically unhealthy. Forty percent of them will develop full-blown T2 diabetes. Seventy-five percent of them have elevated insulin which is responsible for their normal blood sugar.  Therefore, their normal fasting blood sugar levels may not represent a standard for all people to meet, regardless of background diet or activity level.

In short, in the absence of diabetes symptoms and elevated insulin, Baker's high glucose and Hb(a)1c levels may only tell us that after 12 plus hours of fasting, in the absence of dietary carbohydrate, his liver is efficiently generating glucose and exporting it to meet the glucose demands of his brain and to replenish his glycogen stores, and, because he has a very low insulin level, little or none of this blood glucose is becoming adipose tissue. 

What effect may this have on Baker's long term health?  I don't really know, and I don't think anyone else knows either.  Although high fasting blood sugar appears to increase risks of disease in the general population, these risks are in that population also associated with higher insulin levels, higher body fat, and lipid levels that Baker does not exhibit.  

CARDIOVASCULAR AND LIPID MARKERS

Baker's lipoprotein (a) was measured at 2 nmol/L.  That is very, very low (anything below 75 is considered low normal).  Elevated lip (a) is a risk factor for cardiovascular disease.   Baker’s very low Lip (a) indicates very very low risk of heart disease.

His total cholesterol was only 205, just 5 points above the accepted “normal” range.  Here it bears noting that the idea that cholesterol “should” be no more than 200 was put forward by a panel of physicians who were compromised by financial interest in cholesterol-reducing medications.  There is a lack of evidence that total cholesterol below 200 is more protective against cardiovascular disease than one above 200.

In 2009, UCLA researchers reported that "75% of patients hospitalized for heart attacks had cholesterol levels that would indicate they were not at high risk for a cardiovascular event, based on current national cholesterol guidelines."  It should be noted that this study (full text here) was supported by an unrestricted education grant from Merck Schering Plough Partnership.  The authors themselves received grants from AstraZeneca, GlaxoSmithKline, Merck, Sanofi-Aventis, Schering Plough, and Pfizer.

All of these companies are making billions of dollars annually on sales of lipid-reducing drugs.  The paper itself in some paragraphs reads like a promotional brochure for “lipid-lowering therapy.”  The authors claim that LDL contributes to atherosclerosis and that on the basis of their findings physicians should be more aggressive in pharmaceutical reduction of LDL and TC.  But I am sure that their motives, claims and recommendations are all pure as the driven snow.  They wouldn’t be promoting lipid-lowering because they have a financial interest in drugs for lipid lowering would they?

Back to Baker's blood.  A total cholesterol test 5 points above “normal” is also within the range of error expected from lab tests.  In other words, his total cholesterol is just at the high end of the accepted range, and there is a lack of evidence that his cardiovascular risk would be lower if this value was lower.

Moreover, unlike his vegan critics, Baker is aware of the evidence that a serum cholesterol below 200 mg/dL probably has adverse effects on quality of cognitive ability, emotional stability, and thus quality of life. 

The Framingham Study found a significant positive linear association between total cholesterols and measures of verbal fluency, attention/concentration, abstract reasoning, and a composite score measuring multiple cognitive domains.   Subjects with "desirable" TC levels (200 mg/dL) performed less well than participants with borderline-high TC levels (200-239 mg/dL) and participants with high TC levels (>240 mg/dL).  The authors concluded that "lower naturally occurring TC levels are associated with poorer performance on cognitive measures, which place high demands on abstract reasoning, attention/concentration, word fluency, and executive functioning." 

In addition, several studies have linked low cholesterol to increased risk of suicide, suicide again, parasuicide, propensity to violence ("data on this association conform to Hill's criteria for a causal association"),  and antisocial personality (sociopathy or psychopathy).  Apparently cholesterol deprivation has a harmful affect on not only cognition, but also emotion, in at least some people.  Given the importance of cholesterol to the structure and function of the nervous system, this is not a surprising finding.

Perhaps, like me, Baker has had a TC below 200 in the past and from that experience learned that he prefers high cognitive functioning and emotional stability achieved through a meat-based high cholesterol diet to achieving a low LDL of dubious value.

His HDL was 44, which falls into the "borderline low" range (41-59).   However, this level is still above the cut-off for low.  Moreover, Baker reports that low HDL runs in his family, and according to his report his HDL was even lower before adopting the carnivore diet.  This is possible because two very effective ways to raise your HDL levels include to eat a carbohydrate-restricted diet including 3 eggs daily1, 2,3 and to increase your intake of saturated fats.4, 5  In contrast, eating the low fat diet commonly recommended for cardio metabolic health actually decreases HDL.I nearly doubled my HDL in just 30 days by switching from a low fat vegan diet to a VLCHF diet containing more than 6 eggs and plenty of saturated fat daily.

Baker's LDL looks “high” to the untrained eye, but is not concerning to someone who understands the functions and relationships of blood lipids.  As engineer Dave Feldman explains in the following video, the primary role of LDL is to deliver fatty acids to peripheral tissues needing energy.



Baker’s high muscle mass and activity levels means his peripheral tissues have a high demand for energy.  He engages in a large volume of resistance and sprint training which demands large amounts of energy for muscle recovery.  Resting (recovering) muscles obtain 85% of their energy from fatty acids.  Baker has very low adipose levels, so local fat stores can't supply his muscles with much energy.  Therefore, to meet the energy needs of his muscles, his liver has to package a lot of fatty acids in LDLs and export them out to the muscles.  Hence, “high” LDL in his case is probably functional.

His triglycerides were very low (54).  A triglyceride:HDL ratio is a risk factor for “extensive coronary disease.”  In fact, in some studies this ratio shows the strongest relationship with extent of coronary disease, stronger than LDL-C.  Baker’s ratio is 1.2, a very low ratio (below 2.0 is good).  Again, indicating a very low risk for coronary disease

Baker's low triglycerides and trig:HDL ratio suggest it is most likely that his LDL is the large, fluffy type that has a low atherogenicity

Remnant cholesterol is an independent risk factor of cardiovascular disease.  Baker’s Remnant Cholesterol is very low (11 mg/dL) indicating extremely low cardiovascular risk.

If Baker had diabetes, he would have a lipid profile strongly indicating a high risk of cardiovascular disease, because diabetes greatly increases one's cardiovascular disease risk.  The fact that several of Baker's lipid values – Lip(a), trigs, HDL, trig:HDL ratio, and remnant cholesterol – indicate a low or very low risk for cardiovascular disease therefore also probably serves as evidence against a differential diagnosis of diabetes.  

BUN and INFLAMMATION

His BUN (blood urea nitrogen) was only 2 points above the normal range.  This could be measurement error.  However, it is also normal for people who eat high protein diets to have higher BUN.  This does not indicate any disease state.  The National Library of Medicine Medline page on BUN states:

Yes, if your BUN is slightly elevated, talk to your trained health care provider, not the vegan music producer who has a political agenda but no medical training.  If a person is eating a high protein diet, this explains an slightly elevated BUN and rules out the possibility that it represents a disease process. 

Baker's C-reactive protein was 0.6 mg/L.  A level below 1.0 indicates a low level of inflammation. 

His liver function tests were in the normal range.

TESTOSTERONE

Baker's testosterone levels were “low” compared to normal values.  Yet he is obviously not suffering from testosterone deficiency (he has high muscle mass, great strength, deep voice, high spirits, strong drive and motivation, etc.). There are no obvious clinical signs of testosterone deficiency. Once again, testosterone deficiency is indicated by symptoms and signs, not by lab values.

Let us keep in mind here that elevated testosterone in older males has been suggested to be a risk factor for prostate hypertrophy and prostate cancer.  Also, increasing testosterone levels can lead to increased aromatization, resulting in elevated estrogen effects such as gynecomastia.

Further, recent research also suggests that high testosterone in older men may increase the risk of heart disease.  Men in the two highest quintiles of testosterone level had a 2.2 times risk of heart disease compared to those in the lowest. [More here.] That's not a small increase in risk. 

Hence, Baker's maintenance of a low testosterone level without signs of low testosterone function may be more evidence that he has a low risk for heart disease. 

Testosterone is a powerful hormone and the idea that "more is better" has no empirical basis; in fact there is some very good evidence that excess is harmful.  If one can get its maximum secondary sex benefits with a very low dose, this would be biologically wise.

Baker himself believes his numbers may indicate improved testosterone sensitivity.  This is an interesting idea which I believe has merit.  In fact, testosterone or androgen resistance appears to account for the fact that there is a poor correlation between blood testosterone levels and the characteristic symptoms of testosterone deficiency.  Some men have high testosterone levels yet still have symptoms of testosterone deficiency; others have so-called low testosterone levels by have no symptoms of testosterone deficiency.

Testosterone action can be reduced by increased androgen binding, reduced tissue responsiveness, and decreased androgen receptor activity.  Resistance to sex hormones is age-related and may account for the paradox that high levels of testosterone in youth are not associated with prostate disease, but have in some studies have been found linked to prostate cancer and heart disease in elders. 

Youth have high sex hormone levels and high sensitivity to those hormones, resulting in the positive effects of testosterone and estrogen found in young men and women.  If high testosterone itself caused prostate cancer, then young males should have the highest risk of prostate cancer.  They don’t. 

Once secondary sex characteristics are established by the high hormone levels of youth, a fully mature adult should require less of these hormones to maintain those characteristics.  It is natural for testosterone levels to gradually decline with age.  Hence, if testosterone levels either do not decline or rise with age, this may indicate growing resistance to the action of the hormones.

We know that raising T levels artificially (steroids) in a man with health gonads will down-regulate androgen receptors, as expected.  We thus should also expect that increased testosterone sensitivity would result in a decrease of testosterone levels, just as increased insulin sensitivity decreases insulin levels.

Some elders may have high levels of sex hormones because of a low sensitivity to those hormones, just as T2 diabetics have high insulin because of resistance to insulin.  Under these circumstances of sex hormone resistance, tissues dependent on those hormones (breast, prostate, heart, arteries) may become diseased and it may look like high levels are the cause of the disease, when in fact they are a symptom of the underlying hormone resistance.

As discussed above, Kraft has shown that about 80% of the general population has elevated insulin and insulin resistance.  Thus, the normal insulin level for the general population reflects incipient T2 diabetes.  This suggests the possibility that so-called normal testosterone levels in the general population that is known to have high risks of apparently hormone-related cancers (breast cancer, prostate cancer) may actually be too high, reflecting underlying hormone resistance which increases the risk of those hormone-related disorders.  

If this is so, an individual who adopted a lifestyle that eliminates the hormone resistance – whether insulin, testosterone or estrogen resistance – may have a lower than normal level of sex hormones, yet no symptoms of hormone deficiency.  This would represent physiological economy: the body will only produce the amount of testosterone required to produce the secondary sex characteristics.

Just as insulin resistance will by negative feedback cause the pancreas to increase insulin levels in order to overcome the resistance, androgen resistance should by negative feedback induce the body to produce more androgen to attempt to overcome the resistance.  Just as a T2 diabetic has symptoms and signs of insulin deficiency in spite of having too much insulin, a person with testosterone resistance may symptoms of deficiency of testosterone, in spite of having high or excess testosterone.

Conversely, if you have good testosterone sensitivity, you can get the requisite jobs done with much less testosterone, and therefore less chance of adverse effects from high amounts of testosterone.

Also, a high protein, low carbohydrate diet decreases sex hormone binding globlulin (SHBG) synthesis and sex steroid binding.  Conversely, a low fat, low protein high fiber diet (most vegan iterations) increases SHBG  synthesis and sex steroid binding.

Baker is on a very low carbohydrate, very high protein diet.  Therefore, his SHBG levels are likely at a minimum, which means that very likely very little of his testosterone is bound by SHBG.  In other words, he likely has very high free testosterone despite low total testosterone.  Once again, if he has high testosterone sensitivity AND most of his testosterone is free, then he doesn’t need a high (potentially pathological) testosterone level to maintain healthy secondary sex characteristics.

Resistance exercise increases androgen receptor sensitivity in older men,  and Baker engages in heavy resistance training, so this could contribute to a reduced testosterone level.  Increased receptor sensitivity will feedback to the gonads, resulting in lower testosterone output because the more sensitive testosterone receptors are, the less testosterone is required. 

A meat-based diet rich in L- carnitine may also improve testosterone sensitivity and androgen function. In this study, both carnitine ingestion and exogenous testosterone improved androgen function in older males, but testosterone increased prostate volume – a negative effect of increasing testosterone concentrations – whereas carnitine did not.  According to the authors,
"Testosterone and carnitines significantly improved the peak systolic velocity, end-diastolic velocity,resistive index, nocturnal penile tumescence [NPT], International Index of Erectile Function [IIEF-15] score, Depression, Melancholia Scale score, and fatigue scale score.  Carnitines proved significantly more active than testosterone in improving nocturnal penile tumescence and International Index of Erectile Function score.  Testosterone significantly increased the prostate volume and free and total testosterone levels and significantly lowered serum luteinizing hormone; carnitines did not." [Italics added]

The authors concluded:

To repeat: Carnitine supplementation had more positive effects on male function than testosterone supplementation, without increasing hormone levels or causing prostate enlargement, whereas testosterone supplementation promoted prostate enlargement.  Baker eats a lot of red meat, and thereby takes in a large daily dose of carnitine.  This may explain his ability to maintain healthy male function, muscle mass and strength with little testosterone and thus, presumably, little risk of prostate disease.

Finally, we are all different genetically within certain ranges.  Some individuals have large feet, some small feet.  Neither is a disorder.  Similarly, men differ in their blood levels of testosterone and testosterone sensitivity. What works well for one man may not work well for others.  More hormone is not better if it exceeds actual needs.

All that said, hard training can immediately reduce T levels, and overtraining can also reduce T levels.  From what I have seen on his Instagram, Baker might engage in an excessive volume of training, at least at some times.  His testosterone level might be higher if he was not training as much as he does.  This observation also reveals how, again, a physician must use differential diagnosis to determine why any individual's blood values are what they are.  Vegans want Baker's lab values to all be caused exclusively by his carnivorous diet, but his T level is certainly also influenced by his training status.

The bottom line is that testosterone deficiency is a clinical condition, not a lab value.  If there exist no symptoms or signs of testosterone deficiency, then you aren't testosterone deficient, no matter what your blood level.

4/25/18 Update:  I found a study reporting that 25% of elite male athletes had low testosterone levels, which may further support my points here. 

VITAMIN D

Some people have claimed that Baker is vitamin D deficient.  In fact, his vitamin D level was 30 ng/mL, and the normal range is 30-100.  Vegans who have claimed Baker is vitamin D deficient might be interested to learn that John McDougall, M.D. reported in 2011 that his wife Mary McDougall had a vitamin D blood test run in August of 2010.  In McDougall’s words: “She failed, based on commonly reported standards, with a value of 29.6 ng/mL.  Many well-meaning doctors would have told her she was not in good health and in need of supplementation with vitamin D pills, perhaps for a lifetime.”

McDougall goes on to write:
“Mary is not an unusual example of well-sunned people failing this commonly prescribed test. Similar results were found during a study of active young people living in Hawaii with an average sun exposure of 29 hours a week. Even with all that vitamin D-promoting solar radiation, 51 percent of the group failed to meet sufficiency levels of 30 ng/mL.6  The highest reported level was 62 ng/mL and several people had values below 20 ng/mL. Another study of 495 women with an average age of 74 years, living in Hawaii, a geographical area with high environmental UV irradiance, found 44 percent of subjects had vitamin D values of less than 30 ng/mL, but none were below 10 ng/mL; and there was little evidence of seasonal variation of vitamin D levels.7
Any vegans who claim that Baker is vitamin D deficient must then also conclude that Mary McDougall was also found to be vitamin D deficient, by the standards they are uncritically accepting.

I on the other hand think that the studies cited by McDougall provide evidence that the normal vitamin D range (30-100) is inflated, perhaps to encourage doctors to prescribe vitamin D supplements to patients, for the profit of the pharmaceutical companies that make those supplements.

The first study McDougall cited in the above paragraph shows clearly that 51 percent of young people getting abundant sun exposure – 22.4 hours without sunscreen – in Hawaii do not reach blood D levels above 30 ng/mL.  Since none of these people had any signs of vitamin D deficiency, their levels must have been adequate.  This provides good evidence that Baker’s level of 30 ng/mL is quite good, exactly in the mid-range found in a population getting vitamin D from sun exposure.  The authors of this study noted:
“Although the presence of “low” 25(OH)D concentration in this population seems counterintuitive, this might be anticipated from an evolutionary standpoint because the high calcium intake of early humans (27) may have allowed maintenance of calcium homeostasis despite low vitamin D status. Moreover, it is certainly plausible that genetic differences exist in the amount of vitamin D necessary to maintain optimal physiological function. “
The second study found a mean vitamin D level of 32 ng/mL and a lowest of 10 ng/mL in Japanese women who regularly ate vitamin D-rich fish.  Despite the lowest level being 10 ng/mL, the researchers found no evidence of vitamin D deficiency in the population studied.  There was no association between vitamin D status and risk of vertebral fracture in the primary analysis, but “there was a statistically significant increase in risk of vertebral fracture with increasing levels of 25-OHD3 in the secondary analyses adjusted for age, height, weight, and BMD.” Read that again:  Increasing vitamin D levels were associated with an increased risk of vertebral fracture!  Perhaps these were women taking vitamin D supplements; data on their sun exposure, vitamin D and calcium intake were not available..

McDougall points out that there is a lack of evidence for a need for levels higher than 30 ng/mL.  The Institute of Medicine report on vitamin D states: 
"For vitamin D, the 2011 DRIs are based primarily on the integration of bone health outcomes with evidence concerning 25OHD levels, which suggest that levels of 16 ng/ml (40 nmol/liter) meet the needs of approximately half the population (median population requirement, or EAR), and levels of at least 20 ng/ml (50 nmol/liter) meet the needs of at least 97.5% of the population (akin to the RDA)."
Repeat:  Vitamin D levels of at least 20 ng/ml meet the needs of at least 97.5% of the population.  Therefore, unless Shawn Baker is an extreme outlier in vitamin D requirements, his vitamin D status is probably sufficient if not excellent.  I don’t believe there is good evidence to support any contention that his vitamin D status is deficient or harmful. 

SUMMARY

In summary, vegans who have rendered their probably illegal diagnoses of Shawn Baker have no business doing so and have probably only shown their ignorance of human metabolism, biochemistry, and clinical medicine, as well as their uncritical acceptance of normal as healthy, and inability to see what is right in front of their faces (the clinical picture), in their evaluations of Baker's condition.

From the information I obtained from Robb Wolf's interview of Baker in which they revealed some of the results of Baker's blood tests, I find no warrant for the diagnoses I have so far seen vegans passing around. I can't be 100% sure Baker has no underlying pathology, but from what I can see, the chances are that his abnormal blood values simply reflect his efficient metabolic adaptation to an abnormal diet, along with his abnormal muscle mass, strength, and training volume and intensity.  


NOTES

1. Mutungi G, Ratliff G, Publisi M, et al. Dietary Cholsterol from Eggs Increases Plasma HDL Cholesterol in Overweight Men Consuming a Carbohydrate-Restricted Diet. J Nutr 2008 Feb;138(2):272-76. 
2. Schnohr P, Thomsen OO, Riis Hansen P, Boberg-Ans G, Lawaetz H, Weeke T. Egg consumption and high-density-lipoprotein cholesterol. J Intern Med. 1994 Mar;235(3):249-51. PubMed PMID: 8120521.
3. Mayurasakorn K, Srisura W, Sitphahul P, Hongto PO. High-density lipoprotein cholesterol changes after continuous egg consumption in healthy adults. J Med Assoc Thai. 2008 Mar;91(3):400-7. PubMed PMID: 18575296.
4. Hayek T, Ito Y, Azrolan N, et al. Dietary fat increases high density lipoprotein (HDL) levels both by increasing the transport rates and decreasing the fractional catabolic rates of HDL cholesterol ester and apolipoprotein (Apo) A-I. Presentation of a new animal model and mechanistic studies in human Apo A-I transgenic and control mice. Journal of Clinical Investigation. 1993;91(4):1665-1671.
5. Wolf G. High-fat, high-cholesterol diet raises plasma HDL cholesterol: studies on the mechanism of this effect. Nutr Rev. 1996 Jan;54(1 Pt 1):34-5. Review. PubMed PMID: 8919697.
6. Brinton EA, Eisenberg S, Breslow JL. A low-fat diet decreases high density lipoprotein (HDL) cholesterol levels by decreasing HDL apolipoprotein transport rates. Journal of Clinical Investigation. 1990;85(1):144-151.
7.  Binkley N, Novotny R, Krueger D, Kawahara T, Daida YG, Lensmeyer G, Hollis BW, Drezner MK. Low Vitamin D Status despite Abundant Sun Exposure. J Clin Endocrinol Metab. 2007 Jun;92(6):2130-5.  
8.  Pramyothin P, Techasurungkul S, Lin J, Wang H, Shah A, Ross PD, Puapong R, Wasnich RD. Vitamin D status and falls, frailty, and fractures among postmenopausal Japanese women living in Hawaii. Osteoporos Int. 2009 Nov;20(11):1955-62. 

2 comments:

Charles Grashow said...

the general population eats a high carbohydrate plant-based diet

REALLY

Charles Grashow said...

BTW - when will you be posting update blood work??