As early as the 1940’s, research has demonstrated again and again that the rodents that matured and grew the quickest would die earlier than those that matured and grew the slowest . But does this only apply to rats?
Other species of animal were also tested repeatedly with the same results: the faster an animal grew and matured, the younger it died 1 .
Rats! Humans too?
And it probably comes as no surprise that this is now an established fact in humans as well.
Early puberty (in boys and girls) increases our risk of certain cancers, especially breast and prostate cancer2 .
We’ve already looked at the multi-generational impact that high animal protein intake can have on species including humans 3 – where not only is it statistically likely that it will shorten the lifespan of the individual eating the excess quantity of animal protein, but their offspring and the offspring of their offspring will also experience shorter lifespans.
But the idea that hitting puberty earlier means that we are likely to die earlier is probably not something that most of us realise. In the 1840’s, the average age at which girls reached menarche 4 (the first occurrence of menstruation) was about 17 5 . In 1920, it was 14.6; in 1950, 13.1; 1980, 12.5; and in 2010, it had dropped to 10.5. Similar sets of puberty figures have been reported for boys, albeit with a delay of around a year 67 .
Reduce calorie intake to live longer
It’s been proven that restricting the calories an animal can eat, either by underfeeding it or periodically fasting it, it’s possible to significantly prolong its life.
In fact, periodically fasting animals can double their natural life span 89 . Whilst we are not likely to double human life by this means, the evidence is strong that reducing the consumption of animal protein and caloric intake is likely to add years to your life, as can be seen from the largely plant-eating populations which are known to have the longest and healthiest lives – often referred to as the ‘blue zones’ 101112 .
The above chart 13 shows the sort of diet that helps Chinese centenarians to live long and healthy lives.
The above chart 14 should be a wake-up call to us us who live in the UK and USA (position 20 and 31 respectively) – financially rich countries with diets that are robbing most of their citizens of years of healthy life.
Does fasting extend human lifespan?
A 2017 Harvard study1516 concluded that intermittent fasting can play a significant role in extending one’s lifespan. Other studies 17 came to the same conclusion.
This is aside from all the other amazing benefits of water fasting (such as clearing up chronic diseases like obesity, diabetes, ulcerative colitis, Crohn’s, psoriasis, heart disease and cancer), as explained by Drs Michael Klaper 18 , Alan Goldhamer 19 and Joel Fuhrman 20 – a topic that I will cover in more depth shortly.
Final thought
The simple rule of thumb is that what’s best for human longevity is the same thing that’s best for human health in general – lower calories and higher nutrients. This is easily achieved through eating a varied and balanced wholefood plant-based diet.
The 6th annual International Plant-based Nutrition Healthcare Conferenceis set for September 14-17 at the Hilton San Diego Bayfront in San Diego, CA, USA. Such luminaries as Dr. T Colin Campbell, Dr. Michael Greger, Dr Dean Ornish, Dr Michael Klaper and many others will be educating medical practitioners and associated healthcare professionals on how food can heal.
Some of the speakers
The last few blogs have looked at why the mainstream medical profession may be slow to understand the importance of diet and lifestyle changes for our health, and thus why they would not feel able to recommend such changes to their patients. And, in particular, why the optimal WFPB diet would appear too draconian unless one had studied the research supporting its primacy in preventing and treating non-communicable chronic diseases.
So if we are not going to expect the impetus for change to come from the established, government-supported medical system, where do we think the impetus will come from?
Doctor or diet?
Part of the answer is found at grass-roots levels such as at the above-mentioned conference. The speakers are professionals who have had to stand up against their entrenched colleagues and often sacrifice their careers in order to stand by their principles.
These are highly-qualified clinicians who have seen first hand how plant-based diets can radically improve the health outcomes of their patients – preventing, halting and even reversing heart disease, cancer, diabetes, and many other chronic diseases.
Educate or medicate?
All of them are familiar with the wealth of research that shows that plants can heal as well as and often better than pills, and without any negative side-effects.
Pills or plants?
[su_quote cite=”Dean Ornish, MD”]About 75 percent of the $2.8 trillion in annual health care costs in the United States is from chronic diseases that can often be reversed or prevented altogether by a healthy lifestyle. If we put money and effort into helping people make better food and exercise choices, we could improve our health and reduce the cost of health care.[/su_quote]
Most social revolutions throughout history – the abolitionists, the suffragettes – have been started by a small group of informed, principled individuals who needed to fight against an entrenched institutional dogma that only wanted to maintain the status quo – for the benefits of the few and usually at the terrible cost to the many.
Prevention or cure?
The current revolution in western medical practice is being started by a similar small group of highly qualified and informed individuals who often have needed to sacrifice potentially lucrative lifestyles within the system in order to change it. We are somewhere between the stage of ridiculeand violent opposition of the eventual acceptance of the truth that a plant-based diet should be a primary factor in maintaining and treating our health.
Efforts to make changes in clinics and hospitals are oftentrivialised and marginalised by the medical profession.
Efforts to change the law are often crushed by the legal power of BIG Pharma and Big Food.
Efforts to reveal the reality of factory farming are vigorously opposedby business-biased government legislation.
We, too, can play a part in this revolution:
Maintaining our own optimal health through adopting an optimal plant-based diet.
Voting with our shopping trolley – leaving the processed junk and animal foods on the shelves.
Supporting those organisations and individuals who are promoting the benefits of plant-based nutrition – such as PCRM, PBNSG, Nutritionfacts.org, CNS, to name just a few.
Writing to your politicians (UK, USA, EU) and demanding change in healthcare legislation and practice.
Throughout history, we’ve seen that positive social change begins with small numbers of determined and principled individuals who possess only a little power on their own but, at the right time and right place, their combined effort can create a tsunami of change.
The 1958 Delaney Amendment stated that “…no additive is deemed safe if it is found [in “appropriate” tests] to induce cancer when ingested by man or animal…” This US amendment required zero tolerance – that is, no amount of any substance found to be carcinogenic could be added to food. Of course, we know that this noble goal was never achieved and now we have carcinogenic food additives and carcinogenic food processing methods.
£billions are spent researching potential carcinogens found in the environment rather than those found in food. Why is this? Simply, it is easier to get funding for this type of reductionist research than it is to deal with the complexities of human nutrition on a population-wide basis. Also, the so-called Toxic Triad of Big Food, Big Farming and Big Pharma put political and commercial pressure (and lots of it) on research institutions to avoid pointing the finger at powerful food manufacturers, distributors and sellers who make huge profits and contribute huge sums to both government and academic institutions around the world.
The three phases of cancer
Also, there has been an overwhelming emphasis on the first phase of the three phases of cancer (Initiation, Promotion & Progression).
Genetic science appears to be somewhat hamstrung by a particular paradigm. Within this paradigm, consideration is almost solely given to the concept that the only approach we can take is to try and prevent cancers by avoiding the Initiation stage (which happens in a tiny fraction of a second) when DNA is first exposed to carcinogens at the point of cellular reproduction. Once the cancer has passed to the Promotion (years to decades) or Progression (usually years) stages, the seemingly unchallenged consensus appears to be that there is no point in doing anything other than turn to one of the three ugly sisters – surgery, radiation or chemotherapy. As we will see later, there is strong evidence that cancer can be slowed, halted and even reversed completely throughout the Promotion stage and, to perhaps a lesser degree, in the Progression stage of cancer development.
Much of the focus of scientific research, government legislation and media coverage is on individual non-dietary carcinogens (such as radon or asbestos). And even when researchers do deal with diet-related carcinogens, the emphasis for most part is on those carcinogens that are unintentionally included in the food cycle (such as aflatoxin in corn and peanut mould or 2,3,7,8-Tetrachlorodibenzodioxin which is produced during the manufacture of chlorinated hydrocarbons). This tendency can be seen, for instance, in this quote from a section entitled Types of Food Contaminants (my bold highlighted text) in a peer-reviewed paper entitled “Carcinogenic Food Contaminants”:
“There are four primary types of potentially carcinogenic compounds that have been examined to determine if they act as carcinogens in humans. The first are natural products that may be present in food and are unavoidable. For example, the process of creating salted fish produces carcinogens which can not be easily avoided. Second, are natural products that might be avoided such as the contamination of grain with the carcinogenic fungal metabolite aflatoxin, which can be reduced or eliminated using best practices for grain storage. Third, anthropogenic chemicals may be present in food. For instance, 2,3,7,8-tetracholordibenzo-p-dioxin has been inadvertently produced during the manufacture of chlorinated hydrocarbons, but it contaminates the environment, resists degradation, and accumulates in certain foodstuffs. A fourth category of concern is anthropogenic chemicals intentionally added to foods, such as saccharin or food coloring, but these are not addressed in this review because they are not contaminants because they are added intentionally.”
It may be an erroneous assumption, but could this stated avoidance of investigating those dietary carcinogens “intentionally” added to our food be motivated by hidden political/commercial pressures to do so? The paper continues (my bold highlighted text) to this conclusion:
“The accumulation of evidence sufficient to render judgement on food contaminants and human cancer risk is a daunting task…several food contaminants have been confirmed as carcinogenic to humans. Possibly the clearest example is the finding that aflatoxin is a major cause of liver cancer…”
Again, we see a tendency to seek the “clearest” (read “easiest to research”) examples of dietary carcinogens as well as a tendency to miss the elephant in the room – namely, the fact that ALL cancers and other diet-related chronic diseases (e.g. heart disease, diabetes, obesity) are rising around the world at a pace perfectly in parallel with the equal rise in adoption of the Standard American Diet (SAD).
There are reported to be between 80,000 and 100,000 environmental chemicals that would need to be thoroughly tested in order to establish whether or not they each represent a significant cancer risk for humans. Imagine how long that would take? As research teams trawl through these, the focus on the avoidable (i.e. both those intentionally avoided “intentionally added”) dietary carcinogens referred to above would continue to be unwittingly consumed by millions of people. And this is aside from those carcinogens that are not added to foods, but actually ARE the foods, such as our next and main topic casein in dairy.
The animal protein used by Professor T Colin Campbell and his team of researchers was casein, which represents around 85% of all the protein in cow’s milk. He demonstrated that you could turn cancer tumours on and off in rats and mice merely by alternating the amount of protein consumed from 5% to 20% and then from 20% back down to 5% of their total daily calorie intake. Since this research, which is now decades old, he was able to identify the precise mechanisms concerned and how they are involved in all three phases of cancer development.
He is also convinced that other animal proteins have the same detrimental effects – that is, if animal protein intake is increased then cancer risk also increases; but if animal protein intake is reduced then the cancer risk decreases. This can be witnessed in human populations. The following graph shows the example of breast cancer and its geographical spread by country and quantity of average national levels of animal protein (and in this case, also animal fat) consumption. The USA is highlighted in red, but the UK has even higher incidence of breast cancer per capita, reflecting the corresponding higher protein (and fat) intake.
The following chart from The China Study shows female colon cancer rising with meat consumption.
And just to hammer home the correlation between animal protein consumption and incidence of cancer, I have included these further charts from other research:
Assuming a causal rather than a merely correlational relationship between these factors, we can identify the particular protein’s amino acid composition as the specific reason for the adverse effects. Sufficient studies for more than 50 years have shown that the nutritional responses of different proteins are attributed to their differing amino acid compositions; and the differences in nutritional response between animal and plant proteins disappear when any limiting amino acids are restored. Limiting amino acids are those essential amino acids which are present in only small quantities within any given food. The only “food” completely lacking one essential amino acid is gelatin which completely lacks tryptophan. All other foods, as far as I am aware, contain all the essential amino acids, but – and this is the significant point – in varying amounts.
Throughout many experiments over a period of over 30 years, Professor Campbell’s research team found that casein in particular was a powerful promoter of cancer, with two of the major contributory factors being:
increased production of growth hormones, and
elevated body acid load (metabolic acidosis).
Unlike animal proteins such as casein, plant proteins (for instance, the protein in wheat) does not stimulate cancer development. However, as indicated above – when wheat’s limiting amino acid, lysine, is restored to the relevant level, wheat protein acts just the same as casein in terms of cancer promotion.
So, to recap:
animal and plant proteins are not the same
the variation is due to their different amino acid compositions
these different amino acid compositions produce different nutritional responses.
While animal proteins do vary between themselves, any difference is much less than the degree to which they differ from plant proteins as a whole, and there is virtually no overlap between the two groups of protein.
The conventional way in which the so-called “quality” or “completeness” of a protein is determined relates to protein’s efficiency ratio. Thus, plant proteins are described as having LBV (Low Biological Value) while animal proteins are HBV (High Biological Value) depending on how many grams of gain in body weight occur with a given intake of the protein:
Animal proteins cause a greater weight gain over a specified period of time
Plant proteins cause a lesser weight gain over a specified period of time.
Thus,
Egg, meat, cow’s milk, and fish promote a faster rate of growth
Rice, beans and wheat flour promote a slower rate of gain.
So what’s wrong with that?
Nothing, if you want your farm animals to grow rapidly to return the maximum profit over the shortest time; but not if you are a human. Rapid growth in childhood is not a beneficial thing and rapid growth of cancer cells in childhood or adulthood is generally accepted as undesirable.
Cow’s Milk is Baby Calf Growth Fluid
And, as Dr Michael Klaper says: “The purpose of cow’s milk is to turn a 65-pound calf into a 700-pound cow as rapidly as possible. Cow’s milk IS baby calf growth fluid. No matter what you do to it, that is what the stuff is.”
It appears at first sight to be a truly shocking that Professor Campbell should define casein in dairy as “The most relevant cancer promoter ever discovered.”
But it is possible to understand this when one considers the increasingly ubiquitous role that dairy plays in the majority of diets. Dairy products are in everything from pizzas to puddings, sherbets to soups. I needn’t tell you how much the dairy industry promotes its supposed (and largely discredited) health benefits – you just need to turn on the TV or flick through a magazine. And the public at large are so taken in by the claims that it is good for your bones (debatable) and or that it is a health food (debatable).
Dr Neil Barnard from the PCRM (Physicians Committee for Responsible Medicine) goes just as far as Professor Campbell and Dr Michael Klaper. He says “Thanks to these marketing campaigns, milk myths abound in our culture. But science doesn’t support them.” Calling them “white lies” he goes on to attack the myths that the milk industry continues to promote to the public. (Click picture below to read his article, “White Lies? Five Milk Myths Debunked”.)
It occurred to me that one of the reasons that the dairy industry peddles the unsubstantiated myth about milk’s bone-building features is that it is a useful distraction from the potentially catastrophic impact of casein. Maybe I’m just being cynical…In any case, here’s Dr Michael Greger’s view on milk and bone health:
Finally, if you are still in doubt about whether or not people are wise to pour a bit of the white (or red) stuff into their breakfast cereal, I will leave you with a couple of self-explanatory posters about a rather distasteful ingredient that you won’t hear the dairy industry mooing about…
References
T. Colin Campbell. J Nat Sci. Author manuscript; available in PMC 2017 Oct 18. Published in final edited form as: J Nat Sci. 2017 Oct; 3(10): e448. Cancer Prevention and Treatment by Wholistic Nutrition.
David O. Carpenter M.D., Sheila Bushkin-Bedient M.D. Journal of Adolescent Health. Volume 52, Issue 5, Supplement, May 2013, Pages S21-S29. Exposure to Chemicals and Radiation During Childhood and Risk for Cancer Later in Life.
Campbell TC. J Nat Sci. 2017 Oct;3(10). pii: e448. Cancer Prevention and Treatment by Wholistic Nutrition.
Campbell TC. Nutr Cancer. 2017 Aug-Sep;69(6):962-968. doi: 10.1080/01635581.2017.1339094. Epub 2017 Jul 25. Nutrition and Cancer: An Historical Perspective.-The Past, Present, and Future of Nutrition and Cancer. Part 2. Misunderstanding and Ignoring Nutrition.
Campbell TC. Nutr Cancer. 2017 Jul;69(5):811-817. doi: 10.1080/01635581.2017.1317823. Epub 2017 Jun 8. The Past, Present, and Future of Nutrition and Cancer: Part 1-Was A Nutritional Association Acknowledged a Century Ago?
Campbell TM, Campbell TC. Isr Med Assoc J. 2008 Oct;10(10):730-2. The benefits of integrating nutrition into clinical medicine.
Sarter B, Campbell TC, Fuhrman J. Altern Ther Health Med. 2008 May-Jun;14(3):48-53. Effect of a high nutrient density diet on long-term weight loss: a retrospective chart review.
Campbell TC. MedGenMed. 2007;9(3):57. Fail to test the impressive ability of diet to favorably affect long-term health and body weight loss.
Campbell TC. Am J Clin Nutr. 2007 Jun;85(6):1667. Dietary protein, growth factors, and cancer.
Wang Y, Crawford MA, Chen J, Li J, Ghebremeskel K, Campbell TC, Fan W, Parker R, Leyton J. Comp Biochem Physiol A Mol Integr Physiol. 2003 Sep;136(1):127-40. Fish consumption, blood docosahexaenoic acid and chronic diseases in Chinese rural populations.
Feskanich D, Bischoff-Ferrari HA, Frazier AL, Willett WC. JAMA Pediatr. 2014 Jan;168(1):54-60. doi: 10.1001/jamapediatrics.2013.3821. Milk consumption during teenage years and risk of hip fractures in older adults.
Sun Z, Zhang Z, Wang X, Cade R, Elmir Z, Fregly M. Peptides. 2003 Jun;24(6):937-43. Relation of beta-casomorphin to apnea in sudden infant death syndrome.
Fiedorowicz E, Jarmołowska B, Iwan M, Kostyra E, Obuchowicz R, Obuchowicz M. Peptides. 2011 Apr;32(4):707-12. The influence of μ-opioid receptor agonist and antagonist peptides on peripheral blood mononuclear cells (PBMCs).
Kost NV, Sokolov OY, Kurasova OB, Dmitriev AD, Tarakanova JN, Gabaeva MV, Zolotarev YA, Dadayan AK, Grachev SA, Korneeva EV, Mikheeva IG, Zozulya AA. Peptides. 2009 Oct;30(10):1854-60. Beta-casomorphins-7 in infants on different type of feeding and different levels of psychomotor development.
A S Wiley. Biol. 2012 Mar-Apr;24(2):130-8. Cow milk consumption, insulin-like growth factor-I, and human biology: a life history approach. Am J Hum
B C Melnik, S M John, G Schmitz. Nutr J. 2013; 12: 103. Milk is not just food but most likely a genetic transfection system activating mTORC1 signaling for postnatal growth.
C Melnik. J Obes. 2012;2012:197653. Excessive Leucine-mTORC1-Signalling of Cow Milk-Based Infant Formula: The Missing Link to Understand Early Childhood Obesity.
M S Kramer. J Pediatr. 1981 Jun;98(6):883-7. Do breast-feeding and delayed introduction of solid foods protect against subsequent obesity?
B C Melnik. World J Diabetes. 2012 Mar 15;3(3):38-53. Leucine signaling in the pathogenesis of type 2 diabetes and obesity.
A S Wiley. PLoS One. 2011 Feb 14;6(2):e14685. Milk intake and total dairy consumption: associations with early menarche in NHANES 1999-2004.
D S Ludwig, W C Willett. JAMA Pediatr. 2013 Sep;167(9):788-9. Three daily servings of reduced-fat milk: an evidence-based recommendation?
K Arnberg, C Molgaard, K F Michaelsen, S M Jensen, E Trolle, A Larnkjaer. J Nutr. 2012 Dec;142(12):2083-90. Skim milk, whey, and casein increase body weight and whey and casein increase the plasma C-peptide concentration in overweight adolescents.
P Wilde, E Morgan, J Roberts, A Schpok, T Wilson. Physiol Behav. 2012 Aug 20;107(1):172-5. Relationship between funding sources and outcomes of obesity-related research.
Youngman LD, Campbell TC. J Nutr. 1991 Sep;121(9):1454-61. High protein intake promotes the growth of hepatic preneoplastic foci in Fischer #344 rats: evidence that early remodeled foci retain the potential for future growth.
