Navigation Menu

Cow’s Milk – Drinking It at Your Own Risk

Author: Jian Gao, PhD

Editor: Mr. Frederick Malphurs

March 16, 2024

Cow’s milk and dairy products have been touted as an essential food for our health and even existence. Milk production is even considered vital for national security. In reality, the benefits of consuming milk are questionable, yet the harm can be real.

Dubious Benefits

Government agencies, professional associations, and of course the milk industry promote lifelong high milk consumption for bone health of children and adults alike. For instance, on USDA’s MyPlate, the health benefits are listed as:1

  • Improve bone health, especially in children and adolescents when bone mass is being built.
  • Promote bone health and prevent the start of osteoporosis in adults.

The rationale for high milk consumption is to meet the calcium requirement for bone health. However, real life evidence does not support this dogma. In fact, countries with the highest milk consumption and calcium intake tend to have the highest rates of hip fractures, and vice versa.2-5 At the individual level, three system reviews and meta-analyses pooling all the prospective studies together consistently find total dairy product consumption is not associated with the risk of hip fracture in either men or women.6-8

Furthermore, another meta-analysis pulling 5 randomized controlled trials and 12 prospective cohort studies reached the same conclusion – no association between calcium intake and hip fracture risk in women or men.9 The meta-analysis emphasized “Pooled results from randomized controlled trials show no reduction in hip fracture risk with calcium supplementation, and an increased risk is possible.”

More strikingly, a 22-year follow-up study of 96,000 individuals found milk intake during adolescence was correlated with higher risk of hip fracture later in life – every additional glass consumed per day was associated with a 9% increase of risk of hip fracture.10

Milk consumption has also been claimed to be associated with low risks of obesity, diabetes, and heart diseases. But for each study with positive findings there is another one with negative results. The contradictory findings largely stemmed from what food that milk is compared to,2 and confounding factors related to economic status. For instance, the PURE (Prospective Urban and Rural Epidemiology) study published in Lancet in 2018 found high dairy intake was associated with lower risks of major cardiovascular disease, cardiovascular mortality, and total mortality.11 On the other hand, a large prospective study in the US published in BMJ in 2019 found the exact opposite: high risks of cardiovascular mortality, cancer mortality, and total mortality.12

Why did the two large prospective studies come to strikingly opposing conclusions? In addition to methodological issues about comparing milk to what food (e.g., plant protein or processed food),13 more importantly, a key issue that has not been recognized is the two studies examined different populations. Contrary to the study in the US which followed 168,153 women and 49,602 men for up to 32 years, the PURE study followed 136,384 individuals for 9.1 years from 21 mostly developing countries, which were purposely selected for the study because the authors believed most milk and health studies had been done in North America and Europe.

Anyone familiar with diet and life in developing countries would know those routinely consuming milk and dairy products are from the ‘middle’ or ‘upper’ classes with higher income, better education, better nutrition, paying more attention to health, and having better access to healthcare. Of course, they have better health and lower mortality, which almost surely masked any potential ill effects of milk intake. Plus, milk in developing countries, especially in rural areas, may not be as contaminated as in developed countries (e.g., use of growth hormones, antibiotics, and pesticides in feeds). Another potential confounding factor as will be discussed below is the types of milk proteins (caseins) produced by European cows (producing mainly A1 milk) are different from what produced by other cow species in developing countries (producing mainly A2 milk).

Needless to say, as with other topics, there are plethora of meta-analyses and systematic reviews on milk and health pulling individual studies together for an aggregated result. However, when individual studies are misleading, so are the meta-analyses and systematic reviews. It should also be noted the benefit/harm of milk containing both nutritious and deleterious constituents is relative rather than absolute. Milk could be detrimental to those well-nourished, but on the other hand, in regions with food shortage, milk can save many lives. Blindly pulling different studies together is not informative, to say the least.

Potential Risks

Contaminations

Most toxic chemicals including pesticides (e.g., insecticides, herbicides, fungicides, rodenticides) are fat soluble. As a result, cow’s milk, full of fat, is an attractive sanctuary for them. One main source of contamination is from cows’ feeds.14 In the US and around the world, chemical-intensive farming contaminated almost every crop under the sun. According USGS (US Geological Survey),15 “About 1 billion pounds of conventional pesticides are used each year in the United States to control weeds, insects, and other pests.” These pesticides are developed and used as poisons – long-term accumulation of them in our body cannot be good for our health. Indeed, countless studies have found pesticide exposure linked with almost every single disease including cancer.16,17

In addition to the toxins absorbed from feeds, cows are routinely fed or injected with antibiotics, and parasiticides. The scale of antibiotic use is mind boggling – about 160,000 tons of antibiotics were fed to farm animals annually worldwide in 2020.18 Unfortunately, for the same food output, nearly twice as much antibiotics are used in the US compared to European countries (170.8 mg/kg-livestock verse 91.6 mg/kg-livestock).19 Aside from direct health effects on humans, another great concern is the overuse of antibiotics could create superbugs resisting antibiotic treatment.20

Concerns over the toxic pollutants in cow’s milk are warranted. In a recent study, researchers at Emory University collected and analyzed 69 milk samples from nine regions in the US. The study concluded “Current-use antibiotics and pesticides were undetectable in organic but prevalent in conventionally produced milk samples, with multiple samples exceeding federal limits. Higher bGH and IGF-1 levels in conventional milk suggest the presence of synthetic growth hormone.”21

In the US dairy industry, recombinant bovine growth hormone (rBGH), also called recombinant bovine somatotropin (rBST), is routinely injected into dairy cows to increase milk production. rBST is a synthetic hormone created by Monsanto and was approved for use in 1993 by the FDA. In contrast, the European Union, Canada, and many other countries around the world have banned its use due to potential health risks.

With the extensive use of rBGH and novel feed additives, now a cow produces 7.7 gallons of milk on average every day all year around, while a normal cow only produces 1.5 gallons. According to the USDA’s data, the average milk production today is 2,805 gallons or 24,114 pounds per cow per year.22 In order to constantly produce milk, cows have to be pregnant almost all the time through artificial insemination.

And bear in mind, the production of 24,114 pounds of milk by a cow each year is the average. Many cows produce much more. For example, a cow in Wisconsin produced 77,480 pounds (9,009 gallons) of milk in 365 days.23 How can that be good for the health of the cows and people drinking their milk?

The continual injection of rBGH and constant pregnancy stimulates excessive production of many other hormones such as estrogens and progesterone,24 which is linked to variety of disorders such as early puberty.25 In particular, although the direct harm of rBGH has yet to be discovered, studies have clearly demonstrated its use raises the level of IGF-1 (Insulin-like Growth Factor 1) which is associated with the development of several types of cancer such as prostate, breast, and endometrial cancer.2,26-32

Milk Protein and Cancer

In addition to contaminations such as pesticides and hormones, the milk protein itself could be detrimental to human health. There are mainly two types of proteins in cow’s milk: whey (about 20%) and casein (about 80%). It is casein which should be the focus. To understand the issue, we need to meet Dr. Colin Campbell, a prominent nutritional biochemist, professor emeritus at Cornell University. In his academic career, Dr. Campbell was a member of several U.S. National Academy of Sciences expert panels on food nutrition and safety, and he authored and coauthored over 300 scientific papers and several books.  

It all started in the 1960s when Campbell was working on a nationwide project focusing on malnutrition in the Philippines. At the time, malnutrition was loosely defined as deficiency in dietary protein and the solution was to grow more peanuts, which are rich in protein. But the project ran into a snag: unusually high prevalence of liver cancer among Filipino children from the wealthiest families eating the highest protein diet. The culprit was later identified as aflatoxin (one of the most powerful cancer-causing substances) produced by certain fungi found on farm products such as peanuts. So, Campbell had an eye on this poisonous substance.

In 1968, Campbell noticed a striking study published from India. The researchers there studied two groups of rats, where both were administered the same amount of aflatoxin, but one group was fed a diet with 20% casein (the milk protein) while the other group was given 5% of casein. The researchers observed all the rats in the high-protein group developed either liver cancer or precancerous lesions while none of the rats in the low-protein group did.33

At the time, few took the Indian study seriously. When Campbell talked about the Indian finding with his former colleague from MIT, Professor Paul Newberne on a flight from Detroit after attending a conference, Newberne reacted, “They must have gotten the numbers on the animal cages reversed. In no way could a high-protein diet increase the development of cancer.”

As a seasoned and inquisitive researcher, Campbell didn’t let the ‘unbelievable’ finding go. In the ensuing years, Campbell with his colleagues and students were devoted to proving or disproving the India study. Strikingly, all their studies produced the same result as the India study did.34-37 Even more remarkably, they also found plant protein in place of casein did not promote cancer growth at all! 

“Let there be no doubt: cow’s milk protein is an exceptionally potent cancer promoter in rats dosed with aflatoxin,” concluded Campbell. “The fact that this promotion effect occurs at dietary protein levels (10-20%) commonly used both in rodents and humans makes it especially tantalizing – and provocative.”38

The finding spooked the milk industry – a lot of money at stake. So, the special interests sprang into action. According a “leaked” minutes of committee meetings sponsored by the National Dairy Council and the American Meat Institute, an individual was assigned to keep an eye on him.  “… it was disconcerting to find myself on the list of those being spied on,” recalled Campbell.38

To discredit his work, the office of the national president of the American Cancer Society issued a memo alleging “the scientific ‘chair’ of the organization [American Institute for Cancer Research], without naming me, was heading up a group of ‘eight or nine’ discredited physicians, several of whom had spent time in prison,” recalled Campbell. “It was total fabrication. I didn’t even recognize the names of these discredited physicians and had no idea how something so vicious could have gotten started.” And the National Dairy Council also distributed a notice of the memo to its local offices across the country.38  

To attack Campbell’s character and his research method for the findings is beyond preposterous – Campbell was a well-known and well-respected researcher with no vested interest, and the method used in his studies was practically impeccable – the finding that casein promotes cancer growth in rats is rock solid.

The only caveat, an important one, is the finding was based on rats, not humans. It often happens that findings from animals do not apply to humans. To date, of course, no experiments have been done on humans with casein and aflatoxin – we still do not know whether or not casein is a risk for cancer development for humans given most if not all of us unavoidably ingest some aflatoxin from plant food.   

Most of the primary research on casein and cancer by Dr. Campbell and his team was done before 1992. At the time, they did not study what type of casein promoting cancer growth, although casein proteins can be further divided into three types: alpha-, beta-, and kappa-casein. And each of these three types can also be further broken down into subtypes.

A1/A2 Beta-casein and Human Health

In 1993, researchers from New Zealand started to zero in two different types of milk proteins: A1 and A2 beta-casein. What they found is A1 beta-casein in milk is detrimental to human health while A2 is beneficial. To understand the issue, a little biochemistry might be helpful.  

Proteins not only build our body but also run our life – most critically functional or bioactive molecules such as hormones and enzymes in our body are in fact proteins. Amazingly, all proteins in animals and plants are made of 20 amino acids: Alanine (Ala), Arginine (Arg), Asparagine (Asn), Aspartic acid (Asp), Cysteine (Cys), Glutamine (Gln), Glutamic acid (Glu), Glycine (Gly), Histidine (His), Isoleucine (Ile), Leucine (Leu), Lysine (Lys), Methionine (Met), Phenylalanine (Phe), Proline (Pro), Serine (Ser), Threonine (Thr), Tryptophan (Trp), Tyrosine (Tyr), Valine (Val).

Regardless of in humans or animals, all the proteins are synthesized per DNA instructions, a process called gene expression, which dictates what and how many amino acids are used as well as their order in building a specific protein (a string of amino acids). The property and function of proteins including milk protein not only depend on what and how many amino acids are included, but also the order of amino acids in the strings.

Now we can peak into the difference between A1 and A2 beta-casein. Both of them are a string of 209 amino acids. And all the amino acids and their orders are exactly same for A1 and A2 beta-casein except for at position 67 where A1 beta-casein has Histidine (His) while A2 beta-casein has Proline (Pro). This seemly insignificant variation makes all the difference when beta-caseins are digested.

In A2 beta-casein, the bond between Proline (Pro) at position 67 and Isoleucine (Ile) at position 66 is strong and not easily broken up by digest enzymes. On the other hand, in A1 beta-casein, the bond between Histidine (His) at position 67 and Isoleucine (Ile) at position 66 is weak and easily broken up by digest enzymes to form a peptide with seven amino acids, Tyr-Pro-Phe-Pro-Gly-Pro-Ile, which is named as BCM7 (beta-casomorphin-7). Additionally, the bonds between Pro and other amino acids are very strong rendering BCM7 great resistance to further breakdown. Therefore, you get a lot of BCM7 in your digestive system after drinking milk.

By its name beta-casomorphin-7, you can smell something – caso from casein, and morphin from morphine. Indeed, BCM7 has been shown to be a potent opioid peptide – in human body it acts like an opioid.39

The inquiry into A1 and A2 beta-casein was started by Professor Bob Elliott (1934-2020) at Auckland University in New Zealand (for more details, read the scholarly done book Devil in the Milk by Professor Keith Woodford).40,41 In the early 1980s, Elliott already suspected milk protein might play a role in developing type 1 diabetes (T1D).42 As a dedicated pediatrician trying to find answers for childhood maladies, Elliott observed Type 1 diabetes was rare in Samoa, but it was relatively common in Samoan children living in New Zealand – apparently, environmental factors play a major role. In exploring potential risk factors, Elliott noticed children in New Zealand drank a lot more cow’s milk than in Samoa. Was something in cow’s milk the culprit? But later Elliott also realized Type 1 diabetes incidence was very low in parts of East Africa where children had high cow’s milk intake.    

Was the milk in East Africa different from what in New Zealand? Sometime in 1993, Elliott contacted the Dairy Research Institute for hints and Dr. Jeremy Hill answered the call suggesting A1 and A2 beta-caseins were worth exploration. The two became partners in investigating the health effects of A1 and A2 beta-caseins. In one of their preliminary studies, they found 47% of the mice (genetically bred to be prone to type 1 diabetes) indeed got the disorder after being fed with A1 beta-casein, but none of the mice fed with A2 beta-casein after 250 days.43 Furthermore, they also found feeding naloxone (an antagonist neutralizing the effect of opioid) nullified the effect of A1 beta-casein.

The finding was promising, but a follow-up study published in 2002 did not confirm the result (infections and feed contamination have been suggested to be the cause).44 Instead of confirming A1 beta-casein was the culprit, the study found “A milk-free, wheat-predominant diet was highly diabetogenic in three widely separate locations in both animal models.” In other words, gluten was shown to be the problem. Actually, this should not be a surprise because when gluten is partially digested, an opioid peptide named Gliadomorphin (Tyr-Pro-Gln-Pro-Gln-Pro-Phe) similar to BCM7 is also formed.

Unfortunately, there have been no further studies ever since to prove or disprove the findings of these two studies.   

Elliott and colleagues also looked into epidemiological data and found incidence of type 1 diabetes was positively correlated with A1 beta-casein consumption in 19 countries – countries consuming more A1 beta-casein had higher incidence of type 1 diabetes.45,46 Unfortunately, this finding is not conclusive either. In addition to the fact that correlation cannot prove causality, the correlation itself can also be challenged – why are these 19 countries included in the study? Were they selected to prove the authors’ point of view? The authors have yet to answer these challenges.

Taken together, all the circumstantial evidence points to A1 beta-casein as the prime suspect, but unfortunately it has not been convicted in the court of science – the evidence is still beyond reasonable doubt.

Parallel to the investigation of a specific protein in milk (A1 beta-casein), researchers elsewhere have also looked into the association between type 1 diabetes and early childhood exposure to cow’s milk as a whole. Again, the findings are also inconsistent or conflicting. But a large international double-blind randomized controlled trial named TRIGR (Trial to Reduce Insulin-Dependent Diabetes Mellitus in the Genetically at Risk) published in JAMA in 2018 has almost ended the controversy on the relationship between type 1 diabetes onset and childhood exposure to cow’s milk.

TRIGR recruited 2,159 infants with genetic susceptibility to type 1 diabetes between May 2002 and January 2007 in 78 study centers in 15 countries – 1,081 were randomly assigned to the treatment group eating extensively hydrolyzed casein formula (breaking all casein proteins down into small peptides) and 1,078 to a conventional formula with cow’s milk.47 After a median follow-up time of 11.5 years, the study found extensively hydrolyzed casein formula did not reduce the risk of type 1 diabetes at all – the overall conclusion is cow’s milk does not cause type 1 diabetes (T1D) in children.

The TRIGR study could have ended the milk-T1D controversy if it compared the regular formula to BCM7-free formula, but it did not – it did not even report the BCM7 level in the extensively hydrolyzed casein formula.

In short, for the 40-year-old mystery, “The jury is still out on possible links between cows’ milk and type 1 diabetes.”48

Aside from type 1 diabetes, A1 beta-protein has been suspected to induce other maladies such as SIDS (sudden infant death syndrome), autism, immune disorders, cardiovascular disease, and gastrointestinal problems. But all except the last one have ended up with the same fate as type 1 diabetes – inconclusive.39,49-54

Why is it so difficult to either convict or exonerate milk or A1 beta-casein? That is because milk or A1 beta-casein is neither a sufficient nor necessary condition for the development of any of the serious disorders such as type 1 diabetes and autism – individuals can get sick without consuming milk, and people consuming milk do not necessarily get sick. In all probability, milk or BCM7 appears to be one of the risk factors, not the risk factor – other risk factors or triggers are at play too. For instance, without leaky gut (intestinal permeability), BCM7 cannot get into the bloodstream to spook the immune system and further pass BBB (brain blood barrier) to mess with the central nerve system.

And bear in mind, our body systems including the immune and nervous systems are intricately connected and are affected by the total toxic load from environmental chemicals and psychological stress.55 Therefore, how BCM7 behaves in our body is also likely to depend on the toxic chemicals in our body and the stress level, which greatly increases the complexity of convicting BCM7 as guilty.

Regardless of the controversies around the health effects of cow’s milk, one irrefutable fact is that nearly all alternative medicine practitioners (e.g., functional medicine doctors) healing autoimmune diseases, autism, and many other chronic diseases put their patients on the GFCF (gluten free casein free) diet, and not many patients who recovered were not on a GFCF diet.56-61

The Bottomline

From an evolutional perspective, humans only started to consume cow’s milk about 3,000 years ago.54 And we are the only species who drink another species’ milk as part of daily diet after weaning. Given, (1) no nutrients in cow’s milk are not available from other foods, (2) all the hormones and other pollutants in milk, (3) lactose intolerance and allergy for many, and (4) all the potential danger of casein, it does not seem to be worth the risk to drink cow’s milk unless it is A2 and organic.

As to dairy products, the first three problems remain, but the jury has not been even selected for the fourth – different processing methods such as fermentation and heating in producing dairy products could alter the structure and thus the properties of casein differently – there has been little research in this area.    

About the Author and Editor: Jian Gao, PhD, is a healthcare analyst/researcher for the last 27 years who devoted his analytical skills to understanding health sciences and clinical evidence. Mr. Frederick Malphurs is a retired senior healthcare executive in charge of multiple hospitals for decades who dedicated his entire 37 years’ career to improving patient care. Neither of us takes pleasure in criticizing any individuals, groups, or organizations for the failed state of healthcare, but we share a common passion — to reduce unnecessary sufferings inflicted by the so-called chronic or incurable diseases on patients and their loved ones by analyzing and sharing information on root causes, effective treatments, and prevention.

Disclaimer: This article and any contents on this website are informational or educational only and should by no means be considered as a substitute for the advice of a qualified medical professional. It is the patients and caregivers’ solemn responsibility to work with qualified professionals to develop the best treatment plan. The author and editor assume no liability of any outcomes from any treatments or interventions.

References

  1. USDA MyPlate. https://www.myplate.gov/eat-healthy/dairy.
  2. Willett WC, Ludwig DS. Milk and Health. N Engl J Med. 2020 Feb 13;382(7):644-654. doi: 10.1056/NEJMra1903547. PMID: 32053300.
  3. Hegsted DM. Calcium and osteoporosis. J Nutr 1986;116:2316-9.
  4. Hegsted DM. Fractures, calcium, and the modern diet. Am J Clin Nutr 2001;74:571-3.
  5. Campbell TC, Campbell TM. The China Study. 2006. BenBella Books Inc. 6440 N. Central Expressway. Dallas, TX 75206.
  6. Bischoff-Ferrari HA, Dawson-Hughes B, Baron JA, et al. Milk intake and risk of hip fracture in men and women: a meta-analysis of prospective cohort studies. J Bone Miner Res 2011;26:833-9.
  7. Bian S, Hu J, Zhang K, Wang Y, Yu M, Ma J. Dairy product consumption and risk of hip fracture: a systematic review and meta-analysis. BMC Public Health 2018;18:165.
  8. Matía-Martín P, Torrego-Ellacuría M, Larrad-Sainz A, et al. Effects of milk and dairy products on the prevention of osteoporosis and osteoporotic fractures in Europeans and Non-Hispanic whites from North America: a systematic review and updated meta-analysis. Adv Nutr 2019;10:Suppl_2:S120-S143.
  9. Bischoff-Ferrari HA, Dawson-Hughes B, Baron JA, et al. Calcium intake and hip fracture risk in men and women: a meta-analysis of prospective cohort studies and randomized controlled trials. Am J Clin Nutr 2007;86:1780-90.
  10. Feskanich D, Bischoff-Ferrari HA, Frazier AL, Willett WC. Milk consumption during teenage years and risk of hip fractures in older adults. JAMA Pediatr 2014;168:54-60.
  11. Dehghan M, Mente A, Rangarajan S, et al. Prospective Urban Rural Epidemiology (PURE) study investigators. Association of dairy intake with cardiovascular disease and mortality in 21 countries from five continents (PURE): a prospective cohort study. Lancet. 2018 Nov 24;392(10161):2288-2297. doi: 10.1016/S0140-6736(18)31812-9. Epub 2018 Sep 11. PMID: 30217460
  12. Ding M, Li J, Qi L, et al. Associations of dairy intake with risk of mortality in women and men: three prospective cohort studies. BMJ. 2019 Nov 27;367:l6204. doi: 10.1136/bmj.l6204. PMID: 31776125; PMCID: PMC6880246.
  13. https://www.hsph.harvard.edu/nutritionsource/2017/09/08/pure-study-makes-headlines-but-the-conclusions-are-misleading/
  14. Leeman WR, Van Den Berg KJ, Houben GF. Transfer of chemicals from feed to animal products: The use of transfer factors in risk assessment. Food Addit Contam. 2007 Jan;24(1):1-13.
  15. https://www.usgs.gov/centers/ohio-kentucky-indiana-water-science-center/science/pesticides#:~:text=About%201%20billion%20pounds%20of,%2C%20insects%2C%20and%20other%20pests.
  16. Kim KH, Kabir E, Jahan SA. Exposure to pesticides and the associated human health effects. Sci Total Environ. 2017 Jan 1;575:525-535. doi: 10.1016/j.scitotenv.2016.09.009. Epub 2016 Sep 7. PMID: 27614863.
  17. Pathak VM, Verma VK, Rawat BS, et al. Current status of pesticide effects on environment, human health and it’s eco-friendly management as bioremediation: A comprehensive review. Front Microbiol. 2022 Aug 17;13:962619. doi: 10.3389/fmicb.2022.962619. PMID: 36060785; PMCID: PMC9428564.
  18. https://www.theworldcounts.com/challenges/consumption/foods-and-beverages/antibiotics-used-for-livestock
  19. https://www.nrdc.org/sites/default/files/us-livestock-industries-persist-high-intensity-antibiotic-use-ib.pdf
  20. Reardon S. Antibiotic use in farming set to soar despite drug-resistance fears. Nature. 2023 Feb;614(7948):397. doi: 10.1038/d41586-023-00284-x. PMID: 36747098.
  21. Welsh JA, Braun H, Brown N, et al. Production-related contaminants (pesticides, antibiotics and hormones) in organic and conventionally produced milk samples sold in the USA. Public Health Nutr. 2019 Nov;22(16):2972-2980. doi: 10.1017/S136898001900106X. Epub 2019 Jun 26. PMID: 31238996; PMCID: PMC6792142.
  22. https://quickstats.nass.usda.gov/#3436486F-02AB-3C26-9B0E-850D2E5D8BB5
  23. https://www.farmanddairy.com/news/holstein-cow-sets-national-milk-record-of-77480-pounds/392855.html
  24. Maruyama K, Oshima T, Ohyama K. Exposure to exogenous estrogen through intake of commercial milk produced from pregnant cows. Pediatr Int. 2010 Feb;52(1):33-8. doi: 10.1111/j.1442-200X.2009.02890.x. Epub 2009 May 22. PMID: 19496976.
  25. Wiley AS. Milk intake and total dairy consumption: associations with early menarche in NHANES 1999-2004. PLoS One. 2011 Feb 14;6(2):e14685. doi: 10.1371/journal.pone.0014685. PMID: 21347271; PMCID: PMC3038976.
  26. Ganmaa D, Sato A. The possible role of female sex hormones in milk from pregnant cows in the development of breast, ovarian and corpus uteri cancers. Med Hypotheses 2005;65:1028-37.
  27. Harrison S, Lennon R, Holly J, et al. Does milk intake promote prostate cancer initiation or progression via effects on insulin-like growth factors (IGFs)? A systematic review and meta-analysis. Cancer Causes Control 2017;28:497-528.
  28. Ganmaa D, Li XM, Wang J, Qin LQ, Wang PY, Sato A. Incidence and mortality of testicular and prostatic cancers in relation to world dietary practices. Int J Cancer 2002;98:262-7.
  29. Qin LQ, He K, Xu JY. Milk consumption and circulating insulin-like growth factor-I level: a systematic literature review. Int J Food Sci Nutr 2009;60:Suppl 7:330-40.
  30. Shi R, Yu H, McLarty J, Glass J. IGF-I and breast cancer: a meta-analysis. Int J Cancer 2004;111:418-23.
  31. Aune D, Navarro Rosenblatt DA, Chan DS, et al. Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies. Am J Clin Nutr 2015;101:87-117.
  32. Ganmaa D, Cui X, Feskanich D, Hankinson SE, Willett WC. Milk, dairy intake and risk of endometrial cancer: a 26-year follow-up. Int J Cancer 2012;130:2664-71.
  33. Madhavan TV, Gopalan C. The effect of dietary protein on carcinogenesis of aflatoxin. Arch Pathol. 1968 Feb;85(2):133-7.
  34. Appleton BS, Campbell TC. Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic preneoplastic lesion development in the rat. Cancer Res. 1983 May;43(5):2150-4.
  35. Dunaif GE, Campbell TC. Dietary protein level and aflatoxin B1-induced preneoplastic hepatic lesions in the rat. J Nutr. 1987 Jul;117(7):1298-302.
  36. Youngman LD. The growth and development of aflatoxin B1-induced preneoplastic lesions, tumors, metastasis, and spontaneous tumors as they are influenced by dietary protein level, type, and intervention. Ithaca, Cornell University, Ph.D. Dissertation. May, 1990.
  37. Youngman LD, Campbell TC. Inhibition of aflatoxin B1-induced gamma-glutamyltranspeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential. Carcinogenesis. 1992 Sep;13(9):1607-13.
  38. Campbell TC, Campbell TM. The China Study. 2006. BenBella Books Inc. Dallas, TX 75206.
  39. Kuellenberg de Gaudry D, Lohner S, et al. A1- and A2 beta-casein on health-related outcomes: a scoping review of animal studies. Eur J Nutr. 2022 Feb;61(1):1-21. doi: 10.1007/s00394-021-02551-x. Epub 2021 Jun 1. PMID: 34075432; PMCID: PMC8783860.
  40. Woodford K. Devil in the Milk: Illness, Health and the Politics of A1 and A2 Milk. 2009. Chelsea Green Publishing.
  41. Woodford K. Farewell to Sir Bob Elliott. https://keithwoodford.wordpress.com/2021/01/10/farewell-to-sir-bob-elliott/.
  42. Elliott RB, Martin JM. Dietary protein: a trigger of insulin-dependent diabetes in the BB rat? Diabetologia. 1984 Apr;26(4):297-9. doi: 10.1007/BF00283653. PMID: 6376238.
  43. Elliott, R.B., Wasmuth, H.E., Bibby, N.J., & Hill, J. VII.1 – The role of β-casein variants in the induction of insulin-dependent diabetes in the non-obese diabetic mouse and humans. International Dairy Federation special issue, 1997. 445-453.
  44. Beales PE, Elliott RB, Flohé S, et al. A multi-centre, blinded international trial of the effect of A(1) and A(2) beta-casein variants on diabetes incidence in two rodent models of spontaneous Type I diabetes. Diabetologia. 2002 Sep;45(9):1240-6. doi: 10.1007/s00125-002-0898-2. Epub 2002 Jul 19. PMID: 12242456.
  45. Laugesen M, Elliott R. Ischaemic heart disease, Type 1 diabetes, and cow milk A1 beta-casein. N Z Med J. 2003 Jan 24;116(1168):U295. PMID: 12601419.
  46. McLachlan C, Olsson F. Setting the record straight: A1 beta-casein, heart disease and diabetes. N Z Med J. 2003 Mar 14;116(1170):U375. PMID: 12658327.
  47. Writing Group for the TRIGR Study Group; Knip M, Åkerblom HK, Al Taji E, et al. Effect of Hydrolyzed Infant Formula vs Conventional Formula on Risk of Type 1 Diabetes: The TRIGR Randomized Clinical Trial. JAMA. 2018 Jan 2;319(1):38-48. doi: 10.1001/jama.2017.19826. PMID: 29297078; PMCID: PMC5833549.
  48. Ludvigsson J. The jury is still out on possible links between cows’ milk and type 1 diabetes. Acta Paediatr. 2020 Feb;109(2):231-232. doi: 10.1111/apa.14756. Epub 2019 Mar 5. PMID: 30838667.
  49. Chia JSJ, McRae JL, Kukuljan S, Woodford K, Elliott RB, Swinburn B, Dwyer KM. A1 beta-casein milk protein and other environmental pre-disposing factors for type 1 diabetes. Nutr Diabetes. 2017 May 15;7(5):e274. doi: 10.1038/nutd.2017.16. PMID: 28504710; PMCID: PMC5518798.
  50. Küllenberg de Gaudry D, Lohner S, et al. Milk A1 β-casein and health-related outcomes in humans: a systematic review. Nutr Rev. 2019 May 1;77(5):278-306. doi: 10.1093/nutrit/nuy063. PMID: 30722004.
  51. Kay SS, Delgado S, Mittal J, Eshraghi RS, Mittal R, Eshraghi AA. Beneficial Effects of Milk Having A2 β-Casein Protein: Myth or Reality? J Nutr. 2021 May 11;151(5):1061-1072. doi: 10.1093/jn/nxaa454. PMID: 33693747.
  52. Giribaldi M, Lamberti C, Cirrincione S, Giuffrida MG, Cavallarin L. A2 Milk and BCM-7 Peptide as Emerging Parameters of Milk Quality. Front Nutr. 2022 Apr 27;9:842375. doi: 10.3389/fnut.2022.842375. PMID: 35571904; PMCID: PMC9094626.
  53. Cieślińska A, Fiedorowicz E, Rozmus D, et al. Does a Little Difference Make a Big Difference? Bovine β-Casein A1 and A2 Variants and Human Health-An Update. Int J Mol Sci. 2022 Dec 9;23(24):15637. doi: 10.3390/ijms232415637. PMID: 36555278; PMCID: PMC9779325.
  54. de Vasconcelos ML, Oliveira LMFS, Hill JP, Vidal AMC. Difficulties in Establishing the Adverse Effects of β-Casomorphin-7 Released from β-Casein Variants-A Review. Foods. 2023 Aug 22;12(17):3151. doi: 10.3390/foods12173151. PMID: 37685085; PMCID: PMC10486734.
  55. Vermeulen R, Schymanski EL, Barabási AL, Miller GW. The exposome and health: Where chemistry meets biology. Science. 2020 Jan 24;367(6476):392-396. doi: 10.1126/science.aay3164. PMID: 31974245; PMCID: PMC7227413.
  56. Bland JS. The Disease Delusion. 2014. Harper-Collins Publishers. 10 East 53nd Street, New York, NY 10022.
  57. Wahls T. The Wahls Protocol. 2014. The Penguin Group. 375 Hudson Street, New York, NY 10014.
  58. Myers A. The Autoimmune Solution. 2015. Harper-Collins Publishers. 195 Broadway, New York, NY 10007.
  59. Blum S. The Immune System Recovery Plan. Scribner. New York, NY.
  60. McCarthy J, Kartzinel J. Healing and Preventing Autism. 2009. Penguin Group. 375 Hudson Street, New York, NY 10014.
  61. Perlmutter D. Brain Maker. Brain Maker. 2015. Little, Brown and Company. 1290 Avenue of the Americas, New York, NY 10104.
Scroll to Top