Meat vs Wheat: Tales From T Colin Campbell's China Study

OK, probably many readers know that T. Colin Campbell believes that animal foods promote disease and plant foods prevent disease.

In 1996, Campbell and his colleagues published a paper entitled Association of dietary factors and selected plasma variables with sex hormone-binding globulin in rural Chinese women.

In this very interesting report of data from the China study, Campbell et al presented the relationships between various foods and sex hormone-binding globulin (SHBG) in Chinese women.  SHBG binds sex hormones, reducing their effects on tissues.

I am going to quote extensively because I want you to get it from the horse’s mouth, so to speak. In the introduction, Campbell et al write:

“In women, SHBG is clinically implicated in several conditions, ranging from cancer and cardiovascular disease to polycystic ovarian disease and hirsutism (5-8). Lapidus et al (9)

found that a decrease in the concentration of SHBG was a significant risk factor for 12-y overall mortality, concluding that SHBG, androgens, and estrogens should be evaluated as risk factors for cardiovascular disease and death. Suggested positive physiologic regulators of SHBG include testosterone, prolactin, growth hormone, somatomedin-C, and insulin, whereas enterolactone, oral estrogen, and thyroid hormone are potential negative regulators (10).

“Recently however, a growing body of research supports insulin as the primary regulator of SHBG (1 1-14). Furthermore, SHBG has been shown to be an independent predictor of

insulin resistance (15), which is itself suggested to be the common denominator in non-insulin-dependent diabetes mellitus (NIDDM), obesity, hypertension, dyslipidemia, and atherosclerotic

cardiovascular disease, otherwise known in the aggregate as insulin resistance syndrome (IRS) or syndrome X (16, 17). Thus, plasma SHBG itself may be an important indicator for assessing IRS risk.”

In short, the data suggests that low SHBG may play a role in the development of several diseases and associates with increased overall mortality.  Thus, oversimplified, low SHBG=bad, and higher SHBG=good (maybe). 

So Campbell et al went about teasing out associations between foods and SHBG levels in Chinese women using the China Study data.

One of the things they did was throw out data they had collected in Tuoli province, where the people raise animals for milk and meat: 

“Tuoli county from the province of Xinjiang was not included in the analyses because of unreliable data due to measurement problems for several of the covariates of interest.”

Well, that’s convenient.  Apparently, according to Campbell, the people in Tuoli were ‘feasting’ on the day that they collected data. 

I imagine a conversation about this with Dr. Campbell:

Me:  Well, Dr. Campbell, why did you throw out the data from Tuoli?

Campbell:  Because they were feasting when we collected the data.

Me:  Why do you say that they were feasting?

Campbell:  Because they were eating a lot of animal products.

Me:  Don't you expect people who raise animals for milk and meat to eat milk and meat?

Campbell:  Only at feasts.

Me:  What else would pastoralists eat?

Campbell:  Rice and vegetables.

Me:  But they probably can’t grow rice or many vegetables at that latitude and in that climate. That’s why they raise animals!

Campbell:  Look, by definition, if you are eating animal products, you are feasting.  Therefore, I can throw out of the China Study data all data that shows Chinese people eating meat or dairy on a regular basis.

Anyway, leaving aside why Campbell left out of the data set the data from the county that had the highest intake of animal products, let’s take a look at the correlations his team found between foods and SHBG.  In the table below, taken directly from Campbell’s own work, positive numbers means that the food was associated with higher SHBG (good) and negative numbers means that the food was associated with lower SHBG (bad).  Click on image for larger version.

Well, get a load of that.  The “healthywholegrains” wheat, millet, sorghum, and corn, as well as ‘light-colored vegetables,’ carrots, and legumes, primarily soybeans, all have a negative correlation with SHBG whether using the data from the questionnaire or the 3-day diet survey.  That suggests that those things are ‘bad’ for SHBG status and health.

On the other hand, meat, fish, green vegetables, and rice all have a positive correlation with SHBG levels, suggesting these foods are ‘good’ for SHBG and health.

Also note that rice, green vegetables, meat, and fish have negative association with insulin levels, meaning that the women who ate more of these apparently had lower insulin levels.

Further, the negative correlation of legumes is greater than the positive correlation of meat, although not significantly.  This is very interesting given that the Chinese supposedly eat meat very infrequently and legumes very frequently.

This hardly looks like a ringing endorsement of a grain-based vegan diet, regardless of what grain provides the base. 

Huh.  Campbell et al did not miss this, as evident from this paragraph in the text (click on it for a larger version):

Of course, people committed to promoting a vegan diet have a hard time admitting any benefit to eating meat.  Campbell et al try to downplay the protective effect of meat by dismissing its importance in the Chinese diet in this passage:

Click on it to enlarge.

 In other words, they want to say that the beneficial effect of meat isn't important and we can ignore it because Chinese people hardly ever eat meat (except, perhaps, in Tuoli, but we threw that data out).

The paradox for Campbell here is that even those small amounts of meat and fish had strong positive relationships with an apparently protective factor (higher SHBG). In fact, as I noted above, the apparently positive effect of meat had the same magnitude of correlation as the apparently negative effect of legumes (mostly soy) that Chinese people eat quite frequently relative to meat.  This suggests that, per serving, meat has a much greater positive effect than the per serving positive effect of, for example, rice.  

The effect of wheat compared to rice was marked enough that Campbell et al spend a whole, long paragraph discussing the different effects had by rice and wheat on insulin secretion.  From that paragraph, two lines in particular stand out.  The first:

“Wheat may be unique in its relative capacity to stimulate insulin.”

Which they support by referring to several studies establishing a greater insulinogenic effect of wheat compared to rice.  And the second:

“The relative differences in the fatty acid proportions and/or amylose content for wheat and rice may thus be responsible for modulating serum SHBG, triacylglycerols, and insulin. Our study did not find insulin to be predictive of SHBG variation after the effect of the specific foods were adjusted for (particularly rice and wheat).”

In other words, Campbell et al admit that in the China Study data, the strongest predictor for low SHBG status was wheat consumption.

Meanwhile, meat had an inverse, i.e. protective, relationship with SHBG. 

So, there you have it.  According to this paper co-authored by Campbell himself, among Chinese women, wheat aligns with murder and meat aligns with medicine. 

Imagine that.

Diets High in Fish (and Meat) Linked to Stronger Bones

Researchers analyzing data from the Framingham study have reported that people who eat the most fish rich in omega-3 fatty acids have the greatest bone mass.  According to this report from Reuturs:

Women who ate three or more weekly servings of dark fish, such as salmon or mackerel, had smaller amounts of bone loss 4 years later, compared to women who ate less fish.

Men who ate dark fish or tuna at least three times per week also had less bone loss than other men.

Of interest to me, the link between omega-3s and bone density appeared only in people who also had high levels of arachidonic acid, a superunsaturated omega-6 fat richly supplied by meat and eggs:

Looking further into what people ate, the researchers broke down how much of both omega 3 and omega 6 fatty acids people were getting in their diet.

They found that it's not just the omega 3s that are involved in bone density.

High levels of an omega 6 fatty acid, called arachidonic acid, was linked to less bone loss in women - but only when women also consumed higher levels of omega 3 fats.

"It looks like you need to have those in a good balance," Tucker told Reuters Health. "If you have very low levels of arachidonic acid, then you didn't see the benefits of the omega 3s."

 Do a little search with "arachidonic acid and bone mass" and you find other studies supporting the bone-building effect of arachidonic acid.


Weiler found that piglets supplemented with arachidonic acid had higher bone mineral density than non-supplemented piglets.

Blanaru et al and Mollard et al found the same.

Advocates of limiting meat and egg consumption like to use arachidonic acid (AA) as a whipping boy.  They like to claim that AA promotes inflammation.

 Knoch et al started with the hypothesis that AA would increase inflammation in the colon in inflammatory bowel disease, but found on the contrary that "dietary AA, in the present experimental conditions, is not pro-inflammatory, reduces ER stress and protects colonocytes from oxidative stress."

Oops, the "meat is bad" hypothesis proven wrong again. Looks like eating foods rich in AA can build your bones and prevent inflammation and oxidative stress in your colon.

Nevertheless, the government continues to promote it as a "risk factor" for disease.  This table at riskfactor.cancer.gov suggests that the top three sources of the AA "risk factor" in U.S. diets are, in order, chicken, eggs, and beef.

AA only presents a risk if you don't get enough of it.

To build strong bodies 12 ways, eat meat, including fish.  Meat is Medicine. Again.

Surf and turf anyone?

Meat and Fat Diet Delivers Satisfying Results

I really enjoy hearing from people who have taken classes from me and gotten the awesome results you can get by putting paleo principles into practice.

Leslee Ridgeway took nutrition classes from me when I taught at Southwest Institute of Healing Arts,  and has applied the paleo principles in her own life and spread the word.  Here's part of her report: 

For example, I have a four year old and it's very hard to do the low carb thing all the way through with t ball practice and all the societal things we go to that are so backwards with nutrition. I am trying to teach and raise him the best I can without making him feel like he an outcast. Not that it is determined by diet, but it is proving difficult to adjust. His mood and behavior are like night and day difference since getting the fat and protein he needs and low sugar. I have been trying to make some stuff for him that might not be as bad, even though I have decided to pass on it for myself because of my attempts to be closer to a ketogenic diet. 

PS. My family has had a lot of health problems through the years. I suggested everyone test for gluten sensitivity after reading the book you recommended, "Dangerous Grains". So far my sister has been diagnosed with a severe gluten intolerance, and possibly has Celiac, she was referred to a doctor for more testing. She is very young and has a chance at becoming far more healthy because of that (she has thyroid disease). Several others are being tested based on the genetic trends. There are at least 50 people I know that are learning to change their diet because of the things you shared with me, that I in turn share with them.

Kids absolutely will thrive if you feed them meat and fat and limit their sugar intake.   Feed people dangerous grains and they will have a lot of health problems.  This all follows from our ancestral hunter heritage.

Grilled salmon with steamed kale

Keeping Cattle: Cause or Cure for Climate Crisis? Alan Savory's View

Another follow up to my Meat Is Earth Medicine post.  Savory's holistic land management methods have worked in Africa, Australia, and North and South America.  In this video he displays uncommonly astute thinking outside of the box. 


Allan Savory - Keeping Cattle: cause or cure for climate crisis? from Feasta on Vimeo.

Occam's Grazer

Following up on Meat Is Earth Medicine, this speaks for itself.


Occam's Grazer from Raincrow Film on Vimeo.

Crazy Moms and Crying Babies: Brain Damage By Vegan Diet

In 2004, Koebnick et al reported that a "Long-Term Ovo-Lacto Vegetarian Diet Impairs Vitamin B-12 Status in Pregnant Women."  They found that 22% of ovo-lacto vegetarians had demonstrable B-12 deficiency.


In 2011, Gilsing et al reported on the "Serum concentrations of vitamin B12 and folate in British male omnivores, vegetarians, and vegans: results from a cross-sectional analysis of the EPIC-Oxford cohort study."  They found that 52% of vegans had vitamin B-12 deficiency.

Now a 2011 study published in Early Human Development by Goedhart et al--"Maternal vitamin B-12 and folate status during pregnancy and excessive infant crying" -- finds that women with low B-12 status are more likely to have infants that cry more than 3 hours at a time:

Abstract

BACKGROUND: The etiology of excessive infant crying is largely unknown. We hypothesize that excessive infant crying may have an early nutritional origin during fetal development.

AIMS: This study is the first to explore whether (1) maternal vitamin B-12 and folate status during pregnancy are associated with excessive infant crying, and (2) whether and how maternal psychological well-being during pregnancy affects these associations.

STUDY DESIGN: Women were approached around the 12th pregnancy week to complete a questionnaire (n=8266) and to donate a blood sample (n=4389); vitamin B-12 and folate concentrations were determined in serum. Infant crying behavior was measured through a postpartum questionnaire (±3months; n=5218).

SUBJECTS: Pregnant women living in Amsterdam and their newborn child.

OUTCOME MEASURES: Excessive infant crying, defined as crying ≥3h/day on average in the past week.

RESULTS: Multiple logistic regression analysis was performed for 2921 (vitamin B-12) and 2622 (folate) women.Vitamin B-12 concentration (categorized into quintiles) was associated with excessive infant crying after adjustment for maternal age, parity, ethnicity, education, maternal smoking and psychological problems (OR[95%CI]: Q1=3.31[1.48-7.41]; Q2=2.50[1.08-5.77]; Q3=2.59[1.12-6.00]; Q4=2.77[1.20-6.40]; Q5 = reference). Stratified analysis suggested a stronger association among women with high levels of psychological problems during pregnancy. Folate concentration was not associated with excessive infant crying.

CONCLUSIONS: First evidence is provided for an early nutritional origin in excessive infant crying. A low maternal vitamin B-12 status during pregnancy could, in theory, affect infant crying behavior through two potential mechanisms: the methionine-homocysteine metabolism and/or the maturation of the sleep-wake rhythm.

Since meat and fish are the richest sources of B-12, as the Mail Online put it, "a steak for pregnant mothers could stop babies crying."  Forget the stupid final remark by the veg*n nutritionist Yvonne Bishop-Weston.  She proves herself clueless by it.  If anything will destroy your own or your baby's brain, its a vegan diet, not steak, as you will see below.

 I find their report of "a stronger association among women with high levels of psychological problems during pregnancy" intriguing.  Could B-12 deficiency due to meat avoidance increase psychological problems in adults?  Sure enough.

Durand et al reported on a case of "Psychiatric manifestations of vitamin B12 deficiency."

Psychiatric manifestations are frequently associated with pernicious anemia including depression, mania, psychosis, dementia. We report a case of a patient with vitamin B12 deficiency, who has presented severe depression with delusion and Capgras' syndrome, delusion with lability of mood and hypomania successively, during a period of two Months. ...


At admission she was uncooperative, disoriented in time and presented memory and attention impairment and sleep disorders. She seemed sad and older than her real age. Facial expression and spontaneous movements were reduced, her speech and movements were very slow. She had depressed mood, guilt complex, incurability and devaluation impressions. She had a Capgras' syndrome and delusion of persecution....

Further investigations confirmed anemia (hemoglobin=11,4 g/dl) and revealed vitamin B12 deficiency (52 pmol/l) and normal folate level....Vitamin B12 replacement therapy was started with hydroxycobalamin 1 000 ng/day im for 10 days and iron replacement therapy. Her mental state improved dramatically within a few days. After one week of treatment the only remaining symptoms were lability of mood, delusion of persecution, Capgras' syndrome but disappeared totally 9 days after the beginning of the treatment. ...

To illustrate this illness we reviewed the literature regarding psychopathology associated with B12 deficiency. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. The neuropsychiatric severity by vitamin B12 deficiency and the therapeutic efficacy depends on the duration of signs and symptoms.

Conclusion - We recommend consideration of B12 deficiency and serum B12 determinations in all the patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. B12 levels should be evaluated with treatment resistant depressive disorders, dementia, psychosis or risk factors for malnutrition such as alcoholism or advancing age associated with neurological symptoms, anemia, malabsorption, gastrointestinal surgery, parasite infestation or strict vegetarian diet. 

If you search Pub Med you can find lots of articles on psychiatric complications of B-12 deficiency.  Therefore, the finding that women with psychological problems during pregnancy were more likely to have cry babies probably means that those women were more severely B-12 deficient than others.

What else can happen if you don't get enough B-12 during pregnancy?

Lovblad et al reported a case of "Retardation of myelination due to dietary vitamin B12 deficiency:"

Abstract

Vitamin B12 deficiency is known to be associated with signs of demyelination, usually in the spinal cord. Lack of vitamin B12 in the maternal diet during pregnancy has been shown to cause severe retardation of myelination in the nervous system. We report the case of a 14(1)/2-month-old child of strictly vegetarian parents who presented with severe psychomotor retardation. This severely hypotonic child had anemia due to insufficient maternal intake of vitamin B12 with associated megaloblastic anemia. MRI of the brain revealed severe brain atrophy with signs of retarded myelination, the frontal and temporal lobes being most severely affected. It was concluded that this myelination retardation was due to insufficient intake of vitamin B12 and vitamin B12 therapy was instituted. The patient responded well with improvement of clinical and imaging abnormalities. We stress the importance of MRI in the diagnosis and follow-up of patients with suspected diseases of myelination.

 Casella et al reported on "Vitamin B12 deficiency in infancy as a cause of developmental regression."  

Abstract

Vitamin B12 deficiency can cause serious developmental regression, hypotonia and cerebral atrophy in infants. We report a 6-month-old infant, with insidious developmental regression and brain atrophy showed by CT scan, secondarily to vitamin B12 deficiency. His mother was a strict vegetarian and the patient was exclusively breastfed. The clinical symptoms and the brain CT were normalized after vitamin B12 administration.

So we can conclude:

• B-12 deficiency during pregnancy may produce cry babies.
• B-12 deficiency during pregnancy can give your baby brain damage. 
• B-12 deficiency can make you crazy.

So I guess that proves the superiority of a vegan diet, especially a raw one (sarcasm).   

Starting to understand why some long-term unsupplemented vegans can seem a little, well, light headed?  Perhaps some of that gray matter is missing?


Might this explain why it can be so difficult to reason with vegan luminaries such as T. Colin Campbell?


Stay sane, stay smart.  Eat meat. 

Alzheimer's Disease

The European Journal of Internal Medicine just published a paper discussing "Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet."  Authors Seneff, Wainwright, and Mascitelli provided this abstract:

"Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer's disease, and may also be due in large part to this same underlying cause." [Emphasis added]

The idea certainly echos findings that type 2 diabetics (i.e. people with high blood sugar) have an increased risk of diabetes.  In search of an explanation for the link between diabetes and Alzheimer's, Salk Institute researchers did some experiments discussed in this article at Science Daily:

To get at the bottom of the question why diabetes predisposes people to Alzheimer's disease as they age, the Salk researchers Schubert, Burdo and Qi Chen, in collaboration with diabetes expert Nigel Calcutt, a professor in UCSD's Department of Pathology, induced diabetes in young mice, whose genetic background predisposes them to acquire the symptoms of Alzheimer's with old age.

These [high blood sugar] mice suffered damage to blood vessels well before any overt signs of Alzheimer's disease such as nerve cell death or the acquisition of amyloid deposits, the hallmark of the disease, could be detected in their brains. Further experiments revealed that the vascular damage was due to the overproduction of free radicals, resulting in oxidative damage to the cells lining the brain's blood vessels.

"While all people have a low level of amyloid circulating in their blood, in diabetics there may be a synergistic toxicity between the amyloid and high level of blood glucose that is leading to the problems with proper blood vessel formation," says Burdo. [Emphasis added]

 Some researchers have even proposed that Alzheimer's disease is a novel third form of diabetes:

Now scientists at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer's disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer's removes insulin receptors from nerve cells, rendering those neurons insulin resistant...

With other research showing that levels of brain insulin and its related receptors are lower in individuals with Alzheimer's disease, the Northwestern study sheds light on the emerging idea of Alzheimer's being a "type 3" diabetes.

Although some would love to blame the development of Alzheimer's disease on carbohydrates, I can't because we have data from Kitava contradicting it.

The Kitavans appear immune to Alzheimer's while consuming considerably more carbohydrate than the typical American.  Kitavan diets supply nearly 70% of calories as carbohydrate largely from various starchy roots (sweet potatoes, cassava, yam, taro), including a fairly large dose of fructose (perhaps as much as 36 g daily) from tropical fruits (bananas, guava, watermelon, pineapple).

The Kitavan experience provides evidence that they idea that carbohydrates cause Alzheimer's disease is simple hogwash. 

The fact is, diabetes is caused by high fat, high calorie diets, which cause cells to become insulin-resistant.  Yes, too much sugar in the blood promotes Alzheimer's, but elevated blood sugar is a disease of affluence, found only in nations which have high fat, high calorie diets.  It is rare to non-existent among people eating very high carbohydrate, very low fat diets, like the Kitavans, or the Tarahumara.   Hunter-gatherers and pastoralists eating presumably high-fat diets, such as the Inuit or Masai, are only protected by their low caloric intakes.

We have some evidence that vitamin D deficiency may promote Alzheimer's disease.  That study suggests that people with suboptimal D due to inadequate sun exposure have twice the risk of dementia compared to people with optimal D levels. Unfortunately, this study only shows a correlation between low D levels and Alzheimer's, which could be confounded by the so-called healthy subject effect.  That means that people who spend more time in the sun and get more vitamin D might also do something else--like eat less fat--that would protect them from dementia.

We also have evidence that stress promotes Alzheimer's disease:

Stress hormones appear to rapidly exacerbate the formation of brain lesions that are the hallmarks of Alzheimer’s disease, according to researchers at UC Irvine. The findings suggest that managing stress and reducing certain medications prescribed for the elderly could slow down the progression of this devastating disease.

The researchers injected four-month-old transgenic mice with levels of dexamethasone similar to the level of hormones that would be seen in humans under stress. At this young age, there would be little formation of plaques and tangles in the brains of the mice. After one week, the scientists found that the level of beta-amyloid in the brains of the animals compared to what is seen in the brains of untreated eight- to nine-month-old mice, demonstrating the profound consequence of glucocorticoid exposure. When dexamethasone was given to 13-month-old mice that already had some plaque and tangle pathology, the hormone again significantly worsened the plaque lesions in the brain and led to increased accumulation of the tau protein.

 Finally, to name a few explored by researchers, exposure to the following environmental neurotoxins (rare or absent in Kitava) might contribute to the development of Alzheimer's disease:

• organophosphate and organochloride pesticides (occupational exposure)
• lead exposure early in life
• mercury, primarily from dental amalgams (so-called "silver" fillings)

About the last item, although having a large number of amalgam fillings appears to increase the risk of Alzheimer's, I do have to comment that having a large number of amalgam fillings would also be a marker for consumption of a refined food diet, so it could be that both the fillings and the dementia are caused by diet.

Some people believe that a meat-based, low-carb diet may prevent or reverse Alzheimer's. Gasior, Rogawski, and Hartman reviewed the evidence here, stating:

Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer’s disease and Parkinson’s disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury.

In a murine model of Alzheimer's disease, Van der Auwera et al showed that a short-term, high saturated fat, ketogenic diet reduced deposits of toxic amyloid-ß plaque by 25%.  However, they also found that "Despite changes in ketone levels, body weight, and Aβ levels, the KD diet did not alter behavioral measures."  In other words, it didn't modify the disease, which suggests that the ketogenic diet is not beneficial for this disease and further that the plaque may not be the cause of the disease.