Tag: Dr Joel Fuhrman

Being Overweight is Not Just a Cosmetic Issue

The way your body appears from the outside when you’re overweight or obese is a fairly obvious thing that anyone can see; however, what about inside the body? The internal effects of those extra kilos of fat are not so widely appreciated. Dr Joel Fuhrman, in an off-stage video interview 1 while at the Real Truth About Health Conference 2 , gives us the low-down on one of the most devastating effects that being overweight has on our bodies.

Overweight – a serious condition

Being overweight is not a cosmetic issue; rather, it’s a serious medical condition because when you’re overweight, your body becomes insulin sensitive/resistant 3 4 .

Insulin overproduction

Insulin sensitivity/resistance is basically when your pancreas has to produce more insulin in response to eating foods which, if you were not overweight, would not stimulate the pancreas to produce so much.

Thus, just eating oats or an apple will cause the pancreas to go into an insulin-production mode that exceeds what would happen if you were not overweight – according to Dr Fuhrman 5, up to 10 times the amount of insulin can be produced. The insulin wants to put the glucose into cells, but the receptors within cells become blocked from being able to accept the glucose because of the fat within the cell 6 .

This results in the pancreas having to overwork itself just in order to function normally. Any organ will suffer when it is having to overwork for prolonged periods of time, leading to type 2 diabetes and a whole host of chronic diseases.

Insulin promote cancer

Not a lot of people realise that excessive insulin production can cause cancer 7 8 9 .

Insulin promotes angiogenesis

As a fat-storing hormone, insulin can promote angiogenesis – that is, it can promote the growth of new blood vessels. We saw in an earlier blog 10 that reducing angiogenesis is a good thing for reducing the growth of cancers, since they need new blood vessels to feed them and allow them to grow.

Angiogenesis = Production of New Blood Vessels

Dr Fuhrman explains that, for fat cells to grow within the body, they need to excrete angiogenesis-promoting hormones, and insulin further promotes this process. The new blood vessels then feed the fat cells with oxygen and glucose, etc – thus making the fat grow. By doing this, it also promotes other fat cells to grow 11 .

When you’re overweight, the continual circulation of insulin also promotes atherosclerosis 12 and prematurely ages the body 13 .

Fat cells & oestrogen

Another factor comes into play when you are overweight: namely, the higher levels of circulating oestrogen, which is linked to both breast cancer 14 and prostate cancer 15 .

Moderate is okay?

Dr Fuhrman considers that even being moderately overweight is a health risk.

He states quite bluntly:

“There’s no such thing as being a healthy overweight person. If you’re overweight, you’re not at your optimal health. You have to be at your optimal weight to have your optimal health.”

What causes us to be overweight?

He considers that the so-called SAD (Standard American Diet) is what’s really to blame. It keeps us addicted to wanting more food than the body requires.

But when you eat healthy food, you’re flooding yourself with healthy nutrients that the body needs. By eating the right foods, your appetite becomes normal and your weight drops, as he showed in a 2012 research project with 750 individuals who were able to naturally reduce appetite by increasing the nutritional quality of their diets 16 . When you’re body is cleaner, leaner and healthier – fuelled with phytochemicals and antioxidants – you’re not going to have to go through the discomfort of the usual detoxification process that most people experience when they are consuming the ‘wrong’ foods.

Why do most diets fail?

People fail on diets because they try to cut back on calories without increasing the nutritional quality of the foods they eat. And it’s so much easier and more natural to reduce excessive calorie intake when nutrient density increases.

Overweight linked to depression

Research shows 17 18 that when we are overweight, our brains are affected and the likelihood of becoming clinically depressed increases. And this isn’t just because we look in the mirror and don’t like the look of ourselves; it’s linked to biochemical changes within our bodies that change dependent on whether we are at or above our optimal weight.

One in five people in the USA are now classed as mentally ill, and the link between these mental conditions and body weight is clear 19 . And research is starting to uncover 20 a surprising and unwelcome association between increased violent and criminal activity and increased rates of obesity .

Good news – smaller is better

The good news is that normal function of the pancreas can be restored, and type 2 diabetes completely reversed 21 22 23 , through losing weight – ideally through eating an optimally healthy diet consisting totally or mainly of whole plant foods.

Final thoughts

There are so many benefits to being at one’s optimal body weight – both visually and in terms of the internal health of our bodies. It’s good to know that the best way to achieve and maintain this ideal body weight is not through will-power, but can be achieved naturally, healthily and relatively easily by simply eating the right foods for our bodies – that is, foods that are high in nutrients and low in empty calories.

And which diet fits the bill most perfectly? You guessed, a wholefood plant-based diet that avoids added salt, oil and sugar.

Keep an eye out for all the new recipes I regularly add to this website 24 . They’re all guaranteed to be optimally healthy as well as delicious and easy to make.

References

  1. Video Interview: What’s Wrong With Fast Food And Processed Foods? by Joel Fuhrman [↩]
  2. The Hippocrates Real Truth About Health Conference. [↩]
  3. J Clin Invest. 2000 Aug 15; 106(4): 473–481. Obesity and insulin resistance. Barbara B. Kahn and Jeffrey S. Flier. [↩]
  4. Curr Opin Endocrinol Diabetes Obes. 2012 Apr; 19(2): 81–87. What causes the insulin resistance underlying obesity? Olga T. Hardy, Michael P. Czech, and Silvia Corvera. [↩]
  5. Video Interview: What’s Wrong With Fast Food And Processed Foods? by Joel Fuhrman at 3 mins:41 secs. [↩]
  6. Lipids Health Dis. 2015; 14: 121. Published online 2015 Sep 29. doi: 10.1186/s12944-015-0123-1. The role of fatty acids in insulin resistance Barry Sears and Mary Perry. [↩]
  7. Curr Diab Rep. 2013 Apr; 13(2): 213–222. doi: 10.1007/s11892-012-0356-6. The Links Between Insulin Resistance, Diabetes, and Cancer. Etan Orgel, MD, MS and Steven D. Mittelman. [↩]
  8. Diabetes. 2010 May; 59(5): 1129–1131. Diabetes, Insulin Use, and Cancer Risk: Are Observational Studies Part of the Solution–or Part of the Problem? Jeffrey A. Johnson and Edwin A.M. Gale. [↩]
  9. Researchgate: Dagmar Slamenik, University of Cambridge – What is the role of insulin in tumors/cancer development? [↩]
  10. Blood Vessels on the Menu [↩]
  11. JCEM: Link between Adipose Tissue Angiogenesis and Fat Accumulation in Severely Obese Subjects. Amal Y. Lemoine Séverine Ledoux Isabelle Quéguiner Sophie Caldérari Charlotte Mechler Simon Msika Pierre Corvol Etienne Larger. The Journal of Clinical Endocrinology & Metabolism, Volume 97, Issue 5, 1 May 2012, Pages E775–E780 [↩]
  12. Does the Role of Angiogenesis Play a Role in Atherosclerosis and Plaque Instability? [↩]
  13. Circ Res. 2012 Apr 27;110(9):1252-64. Effects of aging on angiogenesis. Lähteenvuo J, Rosenzweig A. [↩]
  14. Breast Cancer Res. 2003; 5(5): 239–247. Oestrogen exposure and breast cancer risk
    Ruth C Travis and Timothy J Key. [↩]
  15. Springerplus. 2016; 5: 522. Oestrogens and oestrogen receptors in prostate cancer. Karolina Kowalska and Agnieszka Wanda Piastowska-Ciesielska. [↩]
  16. Dunaief DM, Fuhrman J, Dunaief JL, Ying. G. Glycemic and cardiovascular parameters improved in type 2 diabetes with the high nutrient density (HND) diet. Open Journal of Preventive Medicine 2012;2(3):364-371. [↩]
  17. Psychiatr Ann. 2012 Aug 1; 42(8): 305–308. The Relationship Between Obesity and Depression Among Adolescents. Deina Nemiary, MD, MPH, Ruth Shim, MD, MPH, Gail Mattox, MD, and Kisha Holden, PhD. [↩]
  18. JAMA: Meta-analysis. March 2010. Overweight, Obesity, and Depression – A Systematic Review and Meta-analysis of Longitudinal Studies. Floriana S. Luppino, MD; Leonore M. de Wit, MS; Paul F. Bouvy, MD, PhD; et al). [↩]
  19. Arch Gen Psychiatry. 2006 Jul; 63(7): 824–830. ASSOCIATION BETWEEN OBESITY AND PSYCHIATRIC DISORDERS IN THE US ADULT POPULATION. Gregory E Simon, MD MPH, Michael Von Korff, ScD, Kathleen Saunders, JD,1 Diana L Miglioretti, PhD, Paul K Crane, MD MPH, Gerald van Belle, PhD, and Ronald C Kessler, PhD. [↩]
  20. J Am Heart Assoc. 2018 Apr 3; 7(7): e008030. Police‐Recorded Crime and Disparities in Obesity and Blood Pressure Status in Chicago. Elizabeth L. Tung, MD, MS,Kristen E. Wroblewski, MS, Kelly Boyd, BS, Jennifer A. Makelarski, PhD, MPH, Monica E. Peek, MD, MPH, and Stacy Tessler Lindau, MD, MAPP. [↩]
  21. EndocrineWeb: Reversing Diabetes with Weight Loss: Stronger Evidence, Bigger Payoff. Written by Kathleen Doheny [↩]
  22. Dr. Neal Barnard’s Program for Reversing Diabetes: The Scientifically Proven System for Reversing Diabetes without Drugs [↩]
  23. The End of Diabetes: The Eat to Live Plan to Prevent and Reverse Diabetes [↩]
  24. WFPB Recipes. [↩]

Nutrients in Plant and Animal Foods

A useful resource for those interested in nutrition is the United States Department of Agriculture (USDA) group of Food Composition Databases 1 . They analyse a massive range of foods and list their nutritional content. In this brief blog, I want to give you a snap-shot of the nutrient values shown within these databases for a given amount of plant-based foods when compared with the same amount of animal-based foods.

The research data

The chart below comes from the USDA databases 2 and from the Journal of Food Composition and Analysis 3 and represents 500 calories of each of the food sources:

The plant-based foods are composed of equal parts of:

  • tomatoes
  • spinach
  • lima beans
  • peas
  • potatoes

The animal-based foods are composed of equal parts of:

  • beef
  • pork
  • chicken
  • whole milk

The exact food listings in the database were:

  • plant-based foods
    • spinach, raw
    • tomatoes, red, ripe, raw, year-round average
    • lima beans, large, mature seeds, raw
    • peas, green, raw
    • potatoes, russet, flesh and skin, raw
  • animal-based foods
    • ground beef, 80% lean meat/20% fat, raw
    • pork, fresh, ground, raw
    • chicken, broilers or fryers, meat and skin, raw
    • milk, dry, whole

Final thoughts

The above speaks for itself. As you can see, there’s much more nutritional value per calorie in plant-foods than in animal-foods, and this is apart from the myriad health problems associated with the latter compared with the former.

As Dr Joel Fuhrman pointed out 4 , Health = Nutrient Intake/Calories. That is, the more nutrient value there is per calorie of the foods you consume, the better health you should expect from your diet; on the other hand, the less nutrient value there is per calorie, the less health benefits you should expect to see.

References

  1. USDA National Nutrient Database for Standard Reference. [↩]
  2. USDA. (2016). National Nutrient Database for Standard Reference Release 28. Retrieved from: http://ndb.nal.usda.gov/ndb/search. [↩]
  3. Journal of Food Composition and Analysis. Volume 12, Issue 3, September 1999, Pages 169-196. [↩]
  4. Health = Nutrient Intake ÷ Calories [↩]

Starting Out on the WFPB Diet – Kitchen Equipment

Expensive kitchen equipment is not needed in order to make great meals on a WFPB diet. This can be seen in the healthiest and longest-lived populations on the planet, such as the Okinawans, who tend to have very simple kitchen equipment. Let’s take a quick look at some basic kitchen kit.

The basics

You need a few pots and pans, whisks, spatulas, spoons, measuring cups, mixing bowls, colander, that’s it. Some of the healthiest populations in the world barely have electricity. So you really just need those basics.

Added convenience

A rice cooker and slow cooker are useful additions, but the one that I tend to use almost daily is a pressure cooker. Drs Joel Fuhrman and Michael Greger make it clear that eating beans every day is one of the healthiest things you can do – particularly when bean-eating is linked to healthy longevity in several epidemiological studies 1 .

I would recommend something like this electric pressure cooker/ multicooker. 2 These are able to cook rice, be pre-programmed on a timer, slow cook, keep food warm and and, for me, most importantly, to switch off automatically once the beans etc are cooked.

We also have a traditional pressure cooker. This will do the job well enough, but you can’t just dump the beans in, press the timer and leave it to do its stuff while you get on with other activities.

Another piece of kit that I use almost every day is a small coffee/spice grinder. I include a tablespoon of ground flaxseeds and chia seeds in my daily diet (along with 6 halves of walnuts) so that I get enough ALA to make the EPA/DHA long-chain omega-3 fatty acids 3 4 that our bodies need. Flaxseeds are so tough that eating them whole means that almost all of them will just pass straight through you. Grinding them (and the chia seeds) ensures that you benefit from their powerful nutrients and phytochemicals – gram for gram, they are also the highest source of lignans5 of any food. As with most foods, freshly grinding them rather than grinding and storing the ground seeds is probably best.

I use a simple coffee/spice grinder6 . It’s efficient and easy to use and clean. I also use it for grinding black peppercorns (to be added daily to the turmeric and tomato juice ‘anti-cancer’ drink) 7 , nuts (to be integrated into salad dressings, sauces, etc) 8 9 , etc.

High-grade blenders, juicers and food processors are, of course, really useful if you can afford them and if you’re going to use them regularly. The cheaper end of the market in these products tend to produce results that are less than satisfactory a lot of the time. This is particularly the case if you are blending/juicing vegetables/fruits with little or no added water.

However, you simply don’t have to spend £100’s or £1000’s on new kitchen equipment to have pretty much all you need to prepare optimally healthy meals.

This is the same when it comes to kitchen tools. It’s always best to spend a bit extra on a really good quality sharp chef’s knife. Not only does it make such a difference in food prep, but it makes it more enjoyable and safer.

Also, having at least two chopping boards (one for fruits and one for veg) is important to avoid your strawberries having that onion or garlic taint! I use flexible, colour-coded polyethylene chopping ‘mats’ 10 . They’re easy to clean and, best of all in my opinion, once the food is chopped up on them, you can bend them and more easily scrape or pour into bowls, pans or whatever.

Other tools include a grater, peeler and a potato masher. By the way, a potato masher isn’t just useful for white potatoes; it’s great for making mash from sweet potatoes, swede, mooli, turnip, carrots, etc, as well as for mashing tofu, beans etc.

Finally, if you’ve never used silicone cookware, you would do well to give them a try – particularly important when eating a WFPBD without any added oils – something that’s strongly recommended 11 12 . I use silicone spatulas, sheets for baking, silicone bread tins for making bread, silicone muffin tins for making … yea, you get the idea 13 .

Silicone – non-stick heaven without any oil needed

That’s about it. There are lots of fads around and many people end up with often expensive kitchen equipment just gathering dust in cupboards.

The most important thing is the quality of the food, not the quality of the gadgets!

References

  1. Pritikin Longevity Center: Want to Live to 100? Eat More Beans! [↩]
  2. PRESSURE KING Pro Digital Pressure Multicooker [↩]
  3. Non-Fish Sources of Omega-3 [↩]
  4. Omega 3 Supplements = Snake Oil [↩]
  5. nutritionfacts.org: flaxseeds and lignans [↩]
  6. Duronic CG250 Premium 250W Electric Coffee Grinder Motor Coffee Bean Spice Nut Stainless Steel Blade Mill [↩]
  7. Why Pepper Boosts Turmeric Blood Levels. Written By Michael Greger M.D. FACLM on February 5th, 2015 [↩]
  8. Dr Furhman’s Almond Balsamic Vinaigrette [↩]
  9. Dr Fuhrman’s Banana Walnut Dressing [↩]
  10. Hygiplas Colour Coded Chopping Mats Set Large [↩]
  11. Olive Oil Injures Endothelial Cells [↩]
  12. No Oil — Not Even Olive Oil! – Caldwell Esselstyn MD [↩]
  13. Tip 14. Use silicone and non-stick cookware [↩]

Our Grandchildren Suffer From Our Meat Consumption

It’s no longer any surprise that your health can be impaired by eating the modern diet of fast food – high in calories and low in nutrients. But did you realise that what you eat may negatively affect the adult health status and lifespans of not only your unborn children, but also your unborn grandchildren? And this is not just scaremongering, it’s based on rigorous multi-species research.

In his excellent book “Fast Food Genocide: How Processed Food Is Killing Us and What We Can Do about It” 1 , Dr Joel Fuhrman explains how evidence is accumulating that: “an unhealthful diet, excess body weight, and especially overeating protein create adverse consequences that are imprinted on genes and passed on to future generations. 2 ”

Mother and father share responsibility

And it’s not just the maternal line that’s involved; the paternal line is also implicated. This means that your diet and lifestyle, as a potential mother or father, can significantly affect not only the infant health but also the adult health of your children and grandchildren, as well as play a part in determining how long they will live. If you’re a parent and/or grandparent, your children’s and grandchildren’s lives will already be influenced (via a processed referred to as ‘transgenerational phenotypic effects’) by the diet and lifestyle choices you made before they were even conceived. This paternal influence is supported both by robust animal experiments 3 4 5 6 7 8 9 and detailed reviews of human observational studies 10 .

A 2014 review 11 concluded that the studies they looked at: “…demonstrate transgenerational associations between grandpaternal/paternal exposures and health outcomes that are most unlikely to be due to ‘cultural’ inheritance/social patterning or genetic inheritance in isolation.”

Pause for thought

There are plenty of studies 12 13 14 15 that look at the complex issue of the precise epigenetic 16 mechanisms involved in causing parental and grandparental influences. However, setting those aside for the purposes of this particular blog, what perhaps should give us considerable pause for thought when we, as adults and, perhaps even more importantly, when our offspring, as they progress through their childhoods, repeatedly consume foods that can have a profound effect, not only on our own health and lifespan, but on the expected health and lifespan of each person’s descendants.

The Överkalix study

On page 130 of Fast Food Genocide, Dr Fuhrman refers to a fascinating study 17) of the grandchildren of people born in Överkalix, Sweden. They also looked at historical records of harvests, food prices, and other information to establish food availability through the generations. Data from a number of previous studies 18 19 20 21 22 were included in the latter research project. These are outlined in the table below along with a brief summary of each study’s findings.

Transgenerational Studies from Överkalix, Sweden Research

The take-away finding

The take-away finding from all this is that a generation’s diet had health effects on three generations. Two groups of people were compared: those who had lived through a period of overabundance of meat and those who had lived through a period of food scarcity. Those who ate a lot of meat in their childhoods produced children and grandchildren who were: “…significantly more likely to develop cardiovascular disease as adults“. On the other hand, those who grew up during periods of relative food scarcity (that is, low meat consumption) had grandchildren who lived considerably longer. And we’re not talking about just a few months longer: “Those people who ate the most meat produced children and grandchildren whose life spans were cut decades short.”

It’s not just junk food – it’s the animal protein

Don’t you find this shocking? And it wasn’t the modern fast-food that was responsible; rather, it was simply eating too much animal protein. We’ve already looked at some of the harm associated with animal protein 23 24 25 , but this puts a whole new multi-generational spin on the damage it can do when eaten to excess – something that is happening pretty much everywhere that the SAD (standard American diet) reaches 26 27 – even if you are a rat on a diet of burger and fries 28 .

It doesn’t make sense…or does it?

It doesn’t seem intuitively obvious why getting lots of meaty protein would be a bad thing for you and your descendants. However, when it’s looked at from an the perspective of evolutionary systematics 29 , it makes perfect sense.

To understand this we need to look at the inextricable relationship between the relative sizes of predator and prey populations.

As Dr Fuhrman states: “Predators and their prey coexist in a circle of interdependence; what happens to one, affects the other. Nature allots a certain amount of each prey to each predator because if predators ate too many of their prey, they would exhaust their food supply and could eat themselves and their prey into extinction.”

Canadian Lynx & snowshoe hare populations

A good example of this is research 30 that looked at how the number of Canadian lynx within a specific area is related to the number of snowshoe hare (which are, more or less, only prey they have in their subarctic environment). Every ten years, there’s a population explosion of hare, which always follows a period of decline in the lynx population. The latter decline in lynx numbers always occurs after the former period of population explosion in their prey.

That is, just after the particular generation of lynx has been able to feast on an overabundance of animal protein (from the hare population explosion), lynx numbers drop – thereby allowing the by-then depleted hare population to recover. The idea that a predator’s life expectancy is shortened by excessive consumption is supported by other research 31 .

Nature protects against extinction.

During the period when a particular prey is low in numbers, it would not be beneficial to predator or prey if that species went extinct – that is, if there were still lots of predators decimating the remaining reduced prey population. So, Nature has engineered it so that too much protein causes changes to the DNA of the predators, causing their life spans AND the life spans of two subsequent generations to be shortened, thereby allowing prey numbers to recover. If the predator numbers recovered too quickly (let’s say in one generation) then they could: “…eat themselves into extinction…This example shows that nature maintains ecological equilibrium by diet-induced DNA changes that alter the expression of predator DNA in response to how much food the predator eats.” 32

Protein-mediated longevity relates to humans as well

It’s not just studies on lynx that show strong evidence for the evolutionarily conserved nature of protein-mediated longevity. There’s extremely strong evidence from other studies 33 that the same mechanism is at play within species ranging from invertebrates to humans. This is a perfect example of the individual being sacrificed for the collective.

Paleo proponents beware

When too much food is available to any predatory species, that species will eat too much food. We don’t normally think of ourselves as predatory, but when we consume meat, that’s exactly what our genes think we are.

Since our modern dietary lifestyle (with the constant availability of pre-packaged meat) is so utterly and uniquely unnatural when viewed from a wider historical perspective, it’s possible to see why those who eat more animal protein have more diseases and die younger – and rather shockingly now to you, perhaps – why their children and their grandchildren will also have more diseases and die younger. Research 34 that looked at Palaeolithic human skeletons showed that few of them survived beyond middle age. And when/where humans did become apex predators – eating most of their calories from hunted animals – the evidence suggests that they died even younger.

Eat plants and live longer

IGF-1 35 production increases when we eat more meat. When we eat plants in place of meat, credible studies 36 37 38 39 40 show that human lifespan increases in length.

Final Thoughts

The foregoing covers a field of research that’s evolving and uncovering more about both the evolutionary systems involved in and the human implications of our current over-consumption of animal protein. And remember, we’re not just talking about big slabs of beef; almost all modern processed foods (except those specifically labelled as being vegan) will contain some animal protein – be it from dairy, fish, insect, mammal or bird origin. Just look at the ingredients on a handful of prepared foods at your local supermarket to get an idea…

Even if we remain sceptical about the above – so that we can continue to indulge in animal protein, irrespective of the potential damage to our health – surely replacing some meat with plants in our and our children’s diets is a sensible thing to do for the health of our descendants.

If you are interested in listening to Dr Fuhrman explain in his own words why certain modern dietary practices are described as a ‘genocide’, I have included a a detailed (1 hour 40 minute) video 41 of one of his lectures from The Truth About Health conference 42 .

Joel Fuhrman Lecture at The truth About Health Conference

References

  1. Fast Food Genocide: How Processed Food Is Killing Us and What We Can Do about It 2017 by Dr Joel Fuhrman MD and Robert Phillips. [↩]
  2. Acta Biotheor. 2001 Mar;49(1):53-9. Longevity determined by paternal ancestors’ nutrition during their slow growth period. Bygren LO1, Kaati G, Edvinsson S. [↩]
  3. Anway MD, Cupp AS, Uzumcu M, Skinner MK. Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science (New York, NY) 2005;308:1466–9 [↩]
  4. Franklin TB, Russig H, Weiss IC, Graff J, Linder N, Michalon A, Vizi S, Mansuy IM. Epigenetic Transmission of the Impact of Early Stress Across Generations. Biol Psychiatry 2010;68:408–15 [↩]
  5. Ng SF, Lin RC, Laybutt DR, Barres R, Owens JA, Morris MJ. Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring. Nature 2010;467:963–6 [↩]
  6. Burdge GC, Slater-Jefferies J, Torrens C, Phillips ES, Hanson MA, Lillycrop KA. Dietary protein restriction of pregnant rats in the F0 generation induces altered methylation of hepatic gene promoters in the adult male offspring in the F1 and F2 generations. Br J Nutr 2007;97:435–9 [↩]
  7. Carone BR, Fauquier L, Habib N, Shea JM, Hart CE, Li R, Bock C, Li C, Gu H, Zamore PD, Meissner A, Weng Z, Hofmann HA, Friedman N, Rando OJ. Paternally induced transgenerational environmental reprogramming of metabolic gene expression in mammals. Cell 2010;143:1084–96 [↩]
  8. Daxinger L, Whitelaw E. Understanding transgenerational epigenetic inheritance via the gametes in mammals. Nat Rev 2012;13:153–62 [↩]
  9. Dias BG, Ressler KJ. Parental olfactory experience influences behavior and neural structure in subsequent generations. Nat Neurosci 2014;17:89–96 [↩]
  10. Pembrey ME, Bygren LO, Golding J. The nature of human transgenerational responses. In: Jirtle HJ, Tyson FL, editors. , ed. Environmental Epigenomics in Health and Disease Epigenetics and Disease Origins. Heidelberg: Springer, 2013:257–1 [↩]
  11. J Med Genet. 2014 Sep; 51(9): 563–572. Human transgenerational responses to early-life experience: potential impact on development, health and biomedical research. Marcus Pembrey, Richard Saffery, Lars Olov Bygren, and Network in Epigenetic Epidemiology. [↩]
  12. Front Genet. 2016; 7: 182. Published online 2016 Oct 24. Nutritional Influence on Epigenetic Marks and Effect on Livestock Production. Brenda M. Murdoch, Gordon K. Murdoch, Sabrina Greenwood, and Stephanie McKay. [↩]
  13. The interaction between epigenetics, nutrition and the development of cancer. Bishop KS, Ferguson LR. Nutrients. 2015 Jan 30;7(2):922-47. doi: 10.3390/nu7020922. Review. PMID: 25647662. [↩]
  14. Sciencedirect: Epigenetics of Aging and Longevity. Translational Epigenetics Vol 4. A volume in Translational Epigenetics. 2018, Pages 229–250. Chapter 11 – Early Nutrition, Epigenetics, and Human Health. Simon C. Langley-Evans, Beverly S. Muhlhausler. [↩]
  15. Nature: Epigenetics: The sins of the father. The roots of inheritance may extend beyond the genome, but the mechanisms remain a puzzle. Virginia Hughes. [↩]
  16. Wikipedia: Epigenetics. [↩]
  17. Cardiovascular and diabetes mortality determined by nutrition during parents’ and grandparents’ slow growth period. G Kaati, LO Bygren & S Edvinsson.
    European Journal of Human Genetics volume 10, pages 682–688 (2002 [↩]
  18. Bygren LO, Kaati G, Edvinsson S. Longevity determined by paternal ancestors’ nutrition during their slow growth period. Acta Biotheor 2001;49:53–9 [↩]
  19. Kaati G, Bygren LO, Edvinsson S. Cardiovascular and diabetes mortality determined by nutrition during parents’ and grandparents’ slow growth period. Eur J Hum Genet 2002;10:682–8 [↩]
  20. Bygren LO, Kaati G, Edvinsson S, Pembrey ME. Reply to senn. Eur J Hum Genet 2006;14:1149–50 [↩]
  21. Senn S. Epigenetics or ephemeral genetics? Eur J Hum Genet 2006;14:1149; author reply 49–50 [↩]
  22. Pembrey ME, Bygren LO, Kaati G, Edvinsson S, Northstone K, Sjostrom M, Golding J, Team AS. Sex-specific, male-line transgenerational responses in humans. Eur J Hum Genet 2006;14:159–66 [↩]
  23. Animal Foods Are The Smoking Gun [↩]
  24. Want Heart Failure? Try the Atkins Diet… [↩]
  25. Animal Protein & Your Kidneys [↩]
  26. nutritionfacts.org article: Standard American Diet [↩]
  27. The Sad ‘Standard American Diet’ Is Taking Over the World by Tove Danovich. [↩]
  28. Scand J Pain. 2017 Oct;17:316-324. doi: 10.1016/j.sjpain.2017.08.009. Epub 2017 Sep 18. The impact of the Standard American Diet in rats: Effects on behavior, physiology and recovery from inflammatory injury.
    Totsch SK, Quinn TL, Strath LJ, McMeekin LJ, Cowell RM, Gower BA, Sorge RE. [↩]
  29. Wikipedia: Evolutionary Systematics or Evolutionary Taxonomy. [↩]
  30. FUNCTIONAL RESPONSES OF COYOTES AND LYNX TO THE SNOWSHOE HARE CYCLE. Mark O’Donoghue Stan Boutin Charles J. Krebs Gustavo Zuleta Dennis L. Murray Elizabeth J. Hofer
    First published: 01 June 1998 https://doi.org/10.1890/0012-9658(1998)079[1193:FROCAL]2.0.CO;2 [↩]
  31. Constant Predator-Prey Ratios: An Arithmetical Artifact? G. Closs, G. A. Watterson and P. J. Donnelly. Ecology Vol. 74, No. 1 (Jan., 1993), pp. 238-243. Published by: Wiley on behalf of the Ecological Society of America. DOI: 10.2307/1939518. [↩]
  32. Fast Food Genocide: How Processed Food Is Killing Us and What We Can Do about It 2017 by Dr Joel Fuhrman MD and Robert Phillips. pp130-1. [↩]
  33. Cell Metab. 2014 Mar 4; 19(3): 407–417. Low Protein Intake is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population. Morgan E. Levine, Jorge A. Suarez, Sebastian Brandhorst, Priya Balasubramanian, Chia-Wei Cheng, Federica Madia, Luigi Fontana, Mario G. Mirisola, Jaime Guevara-Aguirre,j Junxiang Wan, Giuseppe Passarino,f Brian K. Kennedy, Pinchas Cohen, Eileen M. Crimmins, and Valter D. Longo. [↩]
  34. J Natl Med Assoc. 1963 Mar;55:100-6.
    Human paleopathology. GOLDSTEIN MS. [↩]
  35. Wikipedia: IGF-1, Insulin-like growth factor 1 [↩]
  36. Arch Intern Med. 2001 Jul 9;161(13):1645-52. Ten years of life: Is it a matter of choice? Fraser GE1, Shavlik DJ. [↩]
  37. JAMA Intern Med. 2016 Oct 1;176(10):1453-1463. doi: 10.1001/jamainternmed.2016.4182. Association of Animal and Plant Protein Intake With All-Cause and Cause-Specific Mortality. Song M, Fung TT, Hu FB, Willett WC, Longo VD, Chan AT, Giovannucci EL. [↩]
  38. Arch Intern Med. 2012 Apr 9; 172(7): 555–563. Red Meat Consumption and Mortality: Results from Two Prospective Cohort Studies. An Pan, PhD, Qi Sun, MD, ScD, Adam M. Bernstein, MD, ScD, Matthias B. Schulze, DrPH, JoAnn E. Manson, MD, DrPH, Meir J. Stampfer, MD, DrPH, Walter C. Willett, MD, DrPH, and Frank B. Hu, MD, PhD. [↩]
  39. Arch Intern Med. 2009 Mar 23;169(6):562-71. doi: 10.1001/archinternmed.2009.6. Meat intake and mortality: a prospective study of over half a million people. Sinha R, Cross AJ, Graubard BI, Leitzmann MF, Schatzkin A. [↩]
  40. BMC Med. 2013 Mar 7;11:63. doi: 10.1186/1741-7015-11-63. Meat consumption and mortality–results from the European Prospective Investigation into Cancer and Nutrition. Rohrmann S, Overvad K, Bueno-de-Mesquita HB, Jakobsen MU, Egeberg R, Tjønneland A, Nailler L, Boutron-Ruault MC, Clavel-Chapelon F, Krogh V, Palli D, Panico S, Tumino R, Ricceri F, Bergmann MM, Boeing H, Li K, Kaaks R, Khaw KT, Wareham NJ, Crowe FL, Key TJ, Naska A, Trichopoulou A, Trichopoulos D, Leenders M, Peeters PH, Engeset D, Parr CL, Skeie G, Jakszyn P, Sánchez MJ, Huerta JM, Redondo ML, Barricarte A, Amiano P, Drake I, Sonestedt E, Hallmans G, Johansson I, Fedirko V, Romieux I, Ferrari P, Norat T, Vergnaud AC, Riboli E, Linseisen J. [↩]
  41. Joel Fuhrman Video: Fast Food Genocide – Our Nutritional Heritage leading us to Health Tragedies [↩]
  42. The Truth About Health Conference 2018 [↩]

Toxic Hunger vs Real Hunger

The amount of nutrients, rather than the amount of calories, may determine the nature and intensity of hunger – thus helping to explain the paralleled increases in rates of obesity, chronic disease and fast food consumption.

Dr. Joel Fuhrman and his team undertook a study to discover what differences exist in the experience and perception of hunger before and after participants shifted from their previous usual diet to a high nutrient density diet. The following is a precis of the research interspersed with my comments. Apologies in advance for frequent repetition of key aspects, but the study itself expressed and re-expressed what appeared to be similar points but with subtle variations and additions.

Method

This was a retrospective, non-controlled, descriptive study conducted with 768 participants primarily living in the United States who had changed their dietary habits from a low micronutrient to a high micronutrient diet.

Participants completed a survey rating various dimensions of hunger when on their previous usual diet versus the high micronutrient density diet:

  • physical symptoms,
  • emotional symptoms, and
  • location of hunger sensations in the body

Overview

Highly significant differences were found between the two diets:

  • Hunger was not an unpleasant experience while on the high nutrient density diet compared with the low nutrient density diet.
  • Hunger was well tolerated in the high nutrient density diet and occurred with less frequency even when meals were skipped.
  • Nearly 80% of respondents reported that their experience of hunger had changed since starting the high nutrient density diet.
  • 51% reported a dramatic or complete change in their experience of hunger from their normal diet to the high nutrient density diet.

Micronutrient density & hunger

A high micronutrient density diet mitigates the unpleasant aspects of the experience of hunger even though it is lower in calories.

  • Hunger is one of the major impediments to successful weight loss.
  • It’s not simply the caloric content, but more importantly, the micronutrient density of a diet that influences the experience of hunger.
  • A high nutrient density diet, after an initial phase of adjustment during which a person experiences “toxic hunger” due to withdrawal from pro-inflammatory foods, can result in a sustainable eating pattern that leads to weight loss and improved health.
  • A high nutrient density diet provides benefits for long-term health as well as weight loss.
  • The results have important implications in the global effort to control rates of obesity and related chronic diseases.

Micronutrient deficiency & food cravings

One of the common barriers to weight loss is the uncomfortable sensation of hunger that drives overeating and makes dieting fail.

The study is based on Dr. Fuhrman’s clinical experience which clearly suggested that enhancing the micronutrient quality of the diet – even in the context of a substantially lower caloric intake – dramatically mitigates the experience of hunger in his patients.

A diet high in micronutrients appears to decrease food cravings and overeating behaviours.

Sensations such as:

  • fatigue,
  • weakness,
  • stomach cramps,
  • tremors,
  • irritability and headaches,

commonly interpreted as “hunger”, disappear gradually for the majority of people who adopt a high nutrient density diet, and a new, less distressing, sensation (which the researchers label “true” or “throat” hunger) replaces it.

Oxidative stress, toxic metabolites & inflammation

It is well documented [1-4] that a diet low in antioxidant and phytochemical micronutrients leads to heightened oxidative stress and a build-up of toxic metabolites (substances formed in or necessary for metabolism).

It has also been shown [5-10] that a higher intake of nutrient rich plant foods decreases measurable inflammatory by-products.

It is thought that a diet containing an abundance of processed food and low in micronutrient-rich plant foods can create physical symptoms of withdrawal when digestion ceases in between meals.

Toxic hunger

There are two stages of digestion, the anabolic stage which occurs when you are eating and then digesting, and the catabolic stage which begins when you stop eating and your body begins to repair and heal any damage.

The contention is that during the catabolic phase of the digestion and refeeding cycle, when digestive activities cease, these withdrawal symptoms, misperceived as “hunger”, develop from a diet that is inadequate or poor in micronutrients.

These symptoms are called “toxic hunger” by the research team.

Food cravings & dopamine

A “dopaminic high” [11,12] from ingestion of high calorically concentrated sweets and fats has been documented and leads to subsequent craving of these foods.

It is speculated that the discomfort of withdrawal from the toxins mobilised when one tries to refrain from consumption of pro-inflammatory processed foods and animal products may be also be a major contributor to compulsive eating and consequent obesity.

Antioxidants & phytonutrients

Dietary micronutrients such as antioxidants and phytonutrients are required for the body to properly reduce the production and removal of metabolic waste products.

Healthful eating appears to be more effective for long-term weight control because it modifies and diminishes the sensations of withdrawal-related hunger, enabling overweight individuals to be more comfortable even while consuming substantially fewer calories.

Results in charts

The following charts are pretty self-explanatory, showing significant differences between the experience of hunger when eating either a nutrient-poor or -rich diet:

Frequency of “Hunger Pains”

Uncomfortable Hunger between Meals

Discomfort if Meal is Skipped

Frequency of Hunger

Change in Hunger on High Nutrient Density Diet

Mood Affected by Hunger

Irritability When Hungry

Quality of Hunger

Location of Hunger

Discussion

Society & the cycle of overeating

This study provides important insights into hunger in a society characterised by over-consumption of processed food with an excess of calories and deficiency of micronutrients. Such hunger creates a cycle of overeating leading to obesity and is an obstacle for those who attempt to establish a healthy eating pattern and normal BMI.

  • The uncomfortable physical and emotional symptoms of hunger were much less prevalent after a change to the high nutrient density diet.
  • Those who are able to make the change to a high nutrient density diet experienced uncomfortable sensations of hunger less often than they experienced on their previous usual diet.
  • This may explain the previously reported [18] high levels of compliance and successful weight loss with the high nutrient density diet. Their hunger was less often characterised by classic withdrawal symptoms such as headaches, tremors, stomach cramps, and mood changes. Rather, it was more often felt as a throat sensation that was easily tolerated.

The biochemical processes involved

As soon as the intake, digestion and assimilation of food is complete, the catabolic utilisation of glycogen reserves and fatty acid stores begins. Hunger normally increases in intensity as glycogen stores are diminishing toward the end of glycolysis (the breakdown of glucose by enzymes, thus releasing energy), and should not occur at the start of the catabolic phase when glycolysis begins (see glucose response curve diagram below).

The Glucose Response Curve

Toxic vs real hunger

The contention of the researchers is that the uncomfortable symptoms that drive overeating behaviours early in the catabolic phase should be recognised as withdrawal symptoms from a sub-optimal diet and not true hunger.

After the completion of digestive activity, during catabolism, the mobilisation and elimination of cellular waste products are heightened, thus precipitating symptoms commonly thought to be hunger.

In contrast, true hunger occurs much later when glycogen stores near completion, preventing gluconeogenesis (the utilisation of muscle tissue for needed glucose once glycogen stores have been depleted). True hunger protects lean body mass, but does not fuel fat deposition. It exists to protect lean body mass from utilisation as an energy source.

Support of findings from recent research on the physiology of metabolism

  • When a diet is low in dietary antioxidants, phytochemicals and other micronutrients, intra-cellular waste products such as free radicals, advanced glycation end products, lipofuscin, lipid A2E, and others accumulate [9,19].
  • Other studies have demonstrated an adverse impact of low-micronutrient foods containing higher amounts of simple carbohydrates, fats and animal products on levels of inflammatory markers, metabolic by-products and oxidative stress in the body [20,21].
  • It is well established in the scientific literature that these substances contribute to disease [22-25].
  • And that they can be associated with typical withdrawal symptoms, including headaches [26,27].
  • Heightened elimination of these waste products may create symptoms that can be experienced similar to withdrawal from drug addiction [28].
  • In the absence of an adequate intake of phytochemicals and other micronutrients, cellular detoxification is impaired [29] which elevates cellular free radical activity, priming the body with more substrate to induce withdrawal symptoms when digestion ceases.

When eating relieves uncomfortable symptoms

The theory is that the above uncomfortable symptoms, relieved by eating which halts catabolism and arrests the detoxification process, are widely misperceived as hunger. In a society with an abundance of fast food and high rates of obesity, commonly experienced sensations of hunger may actually be symptoms of withdrawal from a diet that is inadequate in micronutrients.

Such a diet creates an excess of pro-inflammatory metabolic waste products as well as an addiction syndrome.

Food addiction as a clinical condition

  • There is growing evidence that food addiction is a clinical pathological condition [30-43].

The results both from this small study and from Dr. Fuhrman’s clinical experience suggest that this addiction is caused by withdrawal symptoms being misread as hunger from pro-inflammatory foods and can be mitigated by consumption of a diet high in anti-inflammatory micronutrients found in vegetables and other micronutrient-rich plant foods.

  • Evidence suggests that overweight individuals build up more inflammatory markers and oxidative stress when fed a low nutrient meal compared to normal weight individuals [20,21].
  • The heightened inflammatory potential in those with a tendency for obesity is marked by increasing levels of lipid peroxidase (the process by which free radicals “steal” electrons from the lipids in cell membranes, resulting in cell damage) and malondialdehyde (a highly reactive compound that occurs naturally and is a marker for oxidative stress) and reduced activation of hepatic detoxification enzymes (these liver enzymes help neutralise and convert toxins into less harmful byproducts, which can still pose a toxic threat to the body if not removed efficiently).[44].

The vicious cycle

People prone to obesity get more withdrawal/hunger symptoms, preventing them from being comfortable in the non-digestive (catabolic) stage where breakdown and mobilisation of toxins is enhanced.

The resulting uncomfortable symptoms drive them to eat again and over-consume calories. It is a vicious cycle promoting continuous (anabolic) digestion, frequent feedings and increased intake of calories.

Chronically overweight people in the typical American food environment feel “normal” only by eating too frequently or by eating a heavy meal, so that the anabolic process of digestion and assimilation continues right up to the beginning of the next meal. Excess calories are needed in order to feel normal.

  • A review of research on companion animals suggested that the introduction of specific micronutrients positively influenced the health status of animals whose natural detoxification systems were compromised, and reduced the accumulation of inflammatory markers [29].

This may explain why those on the high nutrient density diet were able to go for longer periods without feeling “hunger” symptoms.

Relationship between type of foods & hunger intensity/frequency

  • One theory that has been investigated is the glucostatic theory which links dynamic changes in blood glucose with appetitive sensations [45-48].
  • Several studies have explored the relation between the glycaemic index or fibre content of food and satiety, whereas others have examined whether the type or amount of fatty acids, sugars or protein in the diet affect the sense of hunger [49-62].

Results have been inconsistent. This may be due to the unknown variable of micronutrient intake in these studies.

  • Some studies have documented a decrease in appetite with ingestion of greater amounts of fibre and/or micronutrients [49,52,56].
  • A Canadian study found that fasting and postprandial appetite ratings were reduced in women who were supplemented with multivitamins and minerals [63].

Significance of the findings from this and other similar studies

  • Highly significant reductions in blood pressure, LDL cholesterol, fasting glucose and body weight have been reported in persons who have made the change to a high micronutrient diet [18].
  • There is a vast body of research documenting the protective benefit of a micronutrient-rich diet against cancer and cardiovascular disease [1,8,10,24,25,64-77].

Doctors and obese or chronically ill patients

If clinicians can assure their patients with confidence that they will not experience uncomfortable sensations of hunger after the “detoxification” stage is over, they can keep their patients motivated to withstand the withdrawal symptoms they experience early in the dietary transition.

The outcome will be not only substantial and sustainable weight loss, but prevention of many major chronic diseases in patients.

Future studies

There are limitations in this study, but the number of participants and highly significant test statistics provide leads for future studies that are better controlled and prospective in design. It also provides some important clinical insights that can be studied in more detail.

Further studies should explore:

  • The physiological and neurohormonal correlates of “toxic hunger” and of “true hunger“, including measures of oxidative stress and ghrelin levels (nicknamed the ‘hunger hormone’ because it stimulates appetite, increases food intake and promotes fat storage) in people who adhere to the high nutrient density diet and the previous usual diet.
  • How long the typical “withdrawal phase” from the previous usual diet lasts as people shift to the high nutrient density diet.

This information would be valuable in clinical efforts to support those who are making the change to healthier eating patterns.

Study conclusions in brief

  • Significant differences were found in the symptoms, location and unpleasantness of hunger on the high nutrient density diet compared to the participants’ previous usual diet in a large sample of people who had made the shift to a diet high in micronutrients and lower in calories.
  • Hunger is one of the major impediments to successful weight loss.
  • It is not simply the caloric content, but more importantly, the micronutrient density of a diet that influences the experience of hunger.
  • There is an initial phase of adjustment after transitioning from the usual diet to the high nutrient density diet, during which a person experiences “toxic hunger” due to withdrawal from pro-inflammatory foods.
  • A high nutrient density diet can result in a sustainable eating pattern that leads to weight loss and improved health.
  • Further studies are needed to confirm these preliminary findings.
  • These findings may have important implications in the global effort to control rates of obesity and related chronic diseases.

Joe’s final comments

Homeostasis

This study confirms findings from my personal limited research. Namely, that the body craves homeostasis and has all the natural architecture and processes in place to achieve this if, and only if, two conditions are met:

  1. The toxic load on the body is reduced to as low a level as possible, and
  2. There is an optimal dietary intake of sufficient antioxidising, anti-inflammatory, antiangiogenic micronutrients.

Given the foregoing, I believe that the body will heal itself and maintain optimal health if given appropriate nutrients.

Brain/body battle

However, if the body is bombarded with toxic “food”, then it will be continually struggling to reach homeostasis – resulting in symptoms such as those described in the study. Our brains learn to tell us one thing (that we are hungry) while our body is telling us another (that it’s full of toxins and needs to remove them). In the majority of cases nowadays, it appears that the brain wins this battle – as can be seen by the explosion in cases of obesity and diet-related diseases.

Hunger & the transition to a WFPB diet

I have noticed a change in hunger pangs since transitioning to a WFPB diet. Previously, I would experience cravings that simply had to be satisfied – cakes, ice-cream, takeaways, etc seemed like the only solution to a problem over which I had little conscious control. I now experience almost no hunger pangs like this. Eating has become something calm and therapeutic. This is echoed by what I hear reported by friends, family and clients who have similarly made the transition to a WFPB diet.

When we eat foods that are in harmony with our biochemistry, toxins, cancerous cells and fat deposits no longer build up and linger in the body. We feel healthy and the brain is not therefore sent on a wild goose (or chicken McNugget) chase in search of quick dopamine fixes to relieve the bodily discomfort caused by a low-nutrient/high-toxin diet.

Appendix

Low- / High-nutrient value foods

The following chart (see here for more details on ANDI scores) gives an idea of what foods are classified as being either high or low in nutrient value:

These are the sort of nutrients being evaluated within the above study:

ANDI measures calcium; the carotenoids – beta carotene, alpha carotene, lutein, zeaxanthin, and lycopene; fibre; folate; glucosinolates; iron; magnesium; niacin; selenium; vitamins B1 (thiamine), B2 (riboflavin), B6, B12, C, and E; and zinc, plus the ORAC (oxygen radical absorbance capacity) score X 2. Most importantly, the ANDI scores are based on calories, not volume or weight of food, so a lower-calorie food with more nutrients scores higher than a calorie-dense food, which is why foods like iceberg lettuce and kale score high.

 

References

  1. Chobotova K. Aging and Cancer: Converging Routes to Disease Prevention. Integrative Cancer Therapies. 2009;8:115–122. [PubMed]
  2. Devaraj S, Wang-Polagruto J, Polagruto J, Keen CL, Jialal I, Devaraj S, Wang-Polagruto J, Polagruto J, Keen CL, Jialal I. High-fat, energy-dense, fast-food-style breakfast results in an increase in oxidative stress in metabolic syndrome. Metabolism: Clinical & Experimental. 2008;57:867–870.[PMC free article] [PubMed]
  3. Egger G, Dixon J. Inflammatory effects of nutritional stimuli: further support for the need for a big picture approach to tackling obesity and chronic disease. Obesity Reviews. pp. 137–149. [PubMed][Cross Ref]
  4. Esmaillzadeh A, Azadbakht L, Esmaillzadeh A, Azadbakht L. Major dietary patterns in relation to general obesity and central adiposity among Iranian women. Journal of Nutrition. 2008;138:358–363. [PubMed]
  5. Devaraj S, Mathur S, Basu A, Aung HH, Vasu VT, Meyers S, Jialal I, Devaraj S, Mathur S, Basu A. et al. A dose-response study on the effects of purified lycopene supplementation on biomarkers of oxidative stress. Journal of the American College of Nutrition. 2008;27:267–273. [PMC free article][PubMed]
  6. Esmaillzadeh A, Azadbakht L, Esmaillzadeh A, Azadbakht L. Dietary flavonoid intake and cardiovascular mortality. British Journal of Nutrition. 2008;100:695–697. doi: 10.1017/S0007114508945700. [PubMed] [Cross Ref]
  7. Esmaillzadeh A, Kimiagar M, Mehrabi Y, Azadbakht L, Hu FB, Willett WC. Fruit and vegetable intakes, C-reactive protein, and the metabolic syndrome. American Journal of Clinical Nutrition. 2006;84:1489–1497. [PubMed]
  8. O’Keefe JH, Gheewala NM, O’Keefe JO, O’Keefe JH, Gheewala NM, O’Keefe JO. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. Journal of the American College of Cardiology. 2008;51:249–255. doi: 10.1016/j.jacc.2007.10.016. [PubMed][Cross Ref]
  9. Bose KS, Agrawal BK, Bose KSC. Effect of lycopene from tomatoes (cooked) on plasma antioxidant enzymes, lipid peroxidation rate and lipid profile in grade-I hypertension. Annals of Nutrition & Metabolism. 2007;51:477–481. [PubMed]
  10. Thompson HJ, Heimendinger J, Haegele A, Sedlacek SM, Gillette C, O’Neill C, Wolfe P, Conry C. Effect of increased vegetable and fruit consumption on markers of oxidative cellular damage. Carcinogenesis. 1999;20:2261–2266. doi: 10.1093/carcin/20.12.2261. [PubMed] [Cross Ref]
  11. Bello NT, Hajnal A. Dopamine and binge eating behaviors. Pharmacology Biochemistry and behavior. 2010. in press Corrected Proof. [PMC free article] [PubMed]
  12. Berthoud HR. Neural control of appetite: cross-talk between homeostatic and non-homeostatic systems. Appetite. 2004;43:315–317. doi: 10.1016/j.appet.2004.04.009. [PubMed] [Cross Ref]
  13. SurveyMonkey.com. Survey Monkey. Palo Alto, CA;
  14. Friedman MI, Ulrich P, Mattes RD. A Figurative Measure of Subjective Hunger Sensations. Appetite. 1999;32:395–404. doi: 10.1006/appe.1999.0230. [PubMed] [Cross Ref]
  15. Karlsson J, Persson LO, Sjostrom L, Sullivan M. Psychometric properties and factor structure of the Three-Factor Eating Questionnaire (TFEQ) in obese men and women. Results from the Swedish Obese Subjects (SOS) study. International Journal of Obesity & Related Metabolic Disorders: Journal of the International Association for the Study of Obesity. 2000;24:1715–1725. [PubMed]
  16. Lowe MR, Friedman MI, Mattes R, Kopyt D, Gayda C. Comparison of verbal and pictorial measures of hunger during fasting in normal weight and obese subjects. Obesity Research. 2000;8:566–574. doi: 10.1038/oby.2000.73. [PubMed] [Cross Ref]
  17. Gibbons JD. Nonparametric statistics: an introduction. Newbury Park, CA: Sage; 1993.
  18. Sarter B, Campbell T, Fuhrman J. Effect of a high-nutrient density diet on long-term weight loss: a retrospective chart review. Alternative Therapies Health Med. 2008;14:48–51. [PubMed]
  19. Thompson HJ, Heimendinger J, Gillette C, Sedlacek SM, Haegele A, O’Neill C, Wolfe P, Thompson HJ, Heimendinger J, Gillette C. et al. In vivo investigation of changes in biomarkers of oxidative stress induced by plant food rich diets. Journal of Agricultural & Food Chemistry. 2005;53:6126–6132. [PubMed]
  20. Peairs AT, Rankin JW, Peairs AT, Rankin JW. Inflammatory response to a high-fat, low-carbohydrate weight loss diet: effect of antioxidants. Obesity. 2008;16:1573–1578. doi: 10.1038/oby.2008.252.[PubMed] [Cross Ref]
  21. Patel C, Ghanim H, Ravishankar S, Sia CL, Viswanathan P, Mohanty P, Dandona P, Patel C, Ghanim H, Ravishankar S. et al. Prolonged reactive oxygen species generation and nuclear factor-kappaB activation after a high-fat, high-carbohydrate meal in the obese. Journal of Clinical Endocrinology & Metabolism. 2007;92:4476–4479. [PubMed]
  22. Khansari N, Shakiba Y, Mahmoudi M. Chronic inflammation and oxidative stress as a major cause of age-related diseases and cancer. Recent Pat Inflamm Allergy Drug Discov. 2009;3:73–80. doi: 10.2174/187221309787158371. [PubMed] [Cross Ref]
  23. Federico A, Morgillo F, Tuccillo C, Ciardiello F, Loguercio C, Federico A, Morgillo F, Tuccillo C, Ciardiello F, Loguercio C. Chronic inflammation and oxidative stress in human carcinogenesis. International Journal of Cancer. 2007;121:2381–2386. doi: 10.1002/ijc.23192. [PubMed] [Cross Ref]
  24. Willcox JK, Ash SL, Catignani GL, Willcox JK, Ash SL, Catignani GL. Antioxidants and prevention of chronic disease. Critical Reviews in Food Science & Nutrition. 2004;44:275–295. [PubMed]
  25. Guo W, Kong E, Meydani M, Guo W, Kong E, Meydani M. Dietary polyphenols, inflammation, and cancer. Nutrition & Cancer. 2009;61:807–810. [PubMed]
  26. Vives-Bauza C, Anand M, Shirazi AK, Magrane J, Gao J, Vollmer-Snarr HR, Manfredi G, Finnemann SC, Vives-Bauza C, Anand M. et al. The age lipid A2E and mitochondrial dysfunction synergistically impair phagocytosis by retinal pigment epithelial cells. Journal of Biological Chemistry. 2008;283:24770–24780. doi: 10.1074/jbc.M800706200. [PMC free article] [PubMed][Cross Ref]
  27. Bockowski L, Sobaniec W, Kulak W, Smigielska-Kuzia J, Bockowski L, Sobaniec W, Kulak W, Smigielska-Kuzia J. Serum and intraerythrocyte antioxidant enzymes and lipid peroxides in children with migraine. Pharmacological Reports: PR. 2008;60:542–548. [PubMed]
  28. Johnson PM, Kenny PJ, Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. 2010;13:635–641. doi: 10.1038/nn.2519. [PMC free article] [PubMed] [Cross Ref]
  29. Scanlan N. Compromised hepatic detoxification in companion animals and its correction via nutritional supplementation and modified fasting. Alternative Medicine Review. 2001;6(Suppl):S24–37. [PubMed]
  30. Blumenthal DM, Gold MS, Blumenthal DM, Gold MS. Neurobiology of food addiction. Current Opinion in Clinical Nutrition & Metabolic Care. 2010;13:359–365. [PubMed]
  31. Cohen DA, Cohen DA. Neurophysiological pathways to obesity: below awareness and beyond individual control. Diabetes. 2008;57:1768–1773. doi: 10.2337/db08-0163. [PMC free article][PubMed] [Cross Ref]
  32. Corwin RL, Grigson PS, Corwin RL, Grigson PS. Symposium overview–Food addiction: fact or fiction? Journal of Nutrition. 2009;139:617–619. doi: 10.3945/jn.108.097691. [PMC free article][PubMed] [Cross Ref]
  33. Dagher A. The neurobiology of appetite: hunger as addiction. International Journal of Obesity. 2009;33(Suppl 2):S30–33. doi: 10.1038/ijo.2009.69. [PubMed] [Cross Ref]
  34. Davis C, Carter JC. Compulsive overeating as an addiction disorder. A review of theory and evidence. Appetite. 2009;53:1–8. doi: 10.1016/j.appet.2009.05.018. [PubMed] [Cross Ref]
  35. Del Parigi A, Chen K, Salbe AD, Reiman EM, Tataranni PA. Are We Addicted to Food? Obesity. 2003;11:493–495. doi: 10.1038/oby.2003.68. [PubMed] [Cross Ref]
  36. Gosnell BA, Levine AS. Reward systems and food intake: role of opioids. International Journal of Obesity. 2009;33(Suppl 2):S54–58. doi: 10.1038/ijo.2009.73. [PubMed] [Cross Ref]
  37. Ifland JR, Preuss HG, Marcus MT, Rourke KM, Taylor WC, Burau K, Jacobs WS, Kadish W, Manso G. Refined food addiction: a classic substance use disorder. Medical Hypotheses. 2009;72:518–526. doi: 10.1016/j.mehy.2008.11.035. [PubMed] [Cross Ref]
  38. Johnson PM, Kenny PJ. Nat Neurosci. 2010; Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. advance online publication. [PMC free article][PubMed]
  39. Liu Y, von Deneen KM, Kobeissy FH, Gold MS, Liu Y, von Deneen KM, Kobeissy FH, Gold MS. Food addiction and obesity: evidence from bench to bedside. Journal of Psychoactive Drugs. pp. 133–145. [PubMed]
  40. Pelchat ML, Pelchat ML. Food addiction in humans. Journal of Nutrition. 2009;139:620–622. doi: 10.3945/jn.108.097816. [PubMed] [Cross Ref]
  41. Spring B, Schneider K, Smith M, Kendzor D, Appelhans B, Hedeker D, Pagoto S, Spring B, Schneider K, Smith M. et al. Abuse potential of carbohydrates for overweight carbohydrate cravers. Psychopharmacology. 2008;197:637–647. doi: 10.1007/s00213-008-1085-z. [PMC free article][PubMed] [Cross Ref]
  42. Yanover T, Sacco WP. Eating beyond satiety and body mass index. Eating & Weight Disorders: EWD. 2008;13:119–128. [PubMed]
  43. Yeomans MR, Yeomans MR. Alcohol, appetite and energy balance: is alcohol intake a risk factor for obesity? Physiology & behavior. pp. 82–89. [PubMed]
  44. Olusi SO. Obesity is an independent risk factor for plasma lipid peroxidation and depletion of erythrocyte cytoprotectic enzymes in humans. International Journal of Obesity & Related Metabolic Disorders: Journal of the International Association for the Study of Obesity. 2002;26:1159–1164.[PubMed]
  45. Arumugam V, Lee JS, Nowak JK, Pohle RJ, Nyrop JE, Leddy JJ, Pelkman CL, Arumugam V, Lee JS, Nowak JK. et al. A high-glycemic meal pattern elicited increased subjective appetite sensations in overweight and obese women. Appetite. 2008;50:215–222. doi: 10.1016/j.appet.2007.07.003.[PubMed] [Cross Ref]
  46. Fajcsak Z, Gabor A, Kovacs V, Martos E, Fajcsak Z, Gabor A, Kovacs V, Martos E. The effects of 6-week low glycemic load diet based on low glycemic index foods in overweight/obese children–pilot study. Journal of the American College of Nutrition. 2008;27:12–21. [PubMed]
  47. Flint A, Gregersen NT, Gluud LL, Moller BK, Raben A, Tetens I, Verdich C, Astrup A, Flint A, Gregersen NT. et al. Associations between postprandial insulin and blood glucose responses, appetite sensations and energy intake in normal weight and overweight individuals: a meta-analysis of test meal studies. British Journal of Nutrition. 2007;98:17–25. doi: 10.1017/S000711450768297X.[PubMed] [Cross Ref]
  48. Harrington S, Harrington S. The role of sugar-sweetened beverage consumption in adolescent obesity: a review of the literature. Journal of School Nursing. 2008;24:3–12. doi: 10.1177/10598405080240010201. [PubMed] [Cross Ref]
  49. Bosch G, Verbrugghe A, Hesta M, Holst JJ, van der Poel AF, Janssens GP, Hendriks WH. The effects of dietary fibre type on satiety-related hormones and voluntary food intake in dogs. ritish Journal of Nutrition. 2009;102:318–325. doi: 10.1017/S0007114508149194. [PubMed] [Cross Ref]
  50. Cotton JR, Burley VJ, Weststrate JA, Blundell JE, Cotton JR, Burley VJ, Weststrate JA, Blundell JE. Dietary fat and appetite: similarities and differences in the satiating effect of meals supplemented with either fat or carbohydrate. Journal of Human Nutrition & Dietetics. 2007;20:186–199.[PubMed]
  51. Duckworth LC, Gately PJ, Radley D, Cooke CB, King RF, Hill AJ, Duckworth LC, Gately PJ, Radley D, Cooke CB. et al. RCT of a high-protein diet on hunger motivation and weight-loss in obese children: an extension and replication. Obesity. 2009;17:1808–1810. doi: 10.1038/oby.2009.95. [PubMed] [Cross Ref]
  52. Flood-Obbagy JE, Rolls BJ, Flood-Obbagy JE, Rolls BJ. The effect of fruit in different forms on energy intake and satiety at a meal. Appetite. 2009;52:416–422. doi: 10.1016/j.appet.2008.12.001.[PMC free article] [PubMed] [Cross Ref]
  53. Gilbert JA, Drapeau V, Astrup A, Tremblay A, Gilbert JA, Drapeau V, Astrup A, Tremblay A. Relationship between diet-induced changes in body fat and appetite sensations in women. Appetite. 2009;52:809–812. doi: 10.1016/j.appet.2009.04.003. [PubMed] [Cross Ref]
  54. Lemieux S, Lapointe A, Lemieux S, Lapointe A. Dietary approaches to manage body weight. Canadian Journal of Dietetic Practice & Research. 2008;69:3. p following 26. [PubMed]
  55. Lindqvist A, Baelemans A, Erlanson-Albertsson C, Lindqvist A, Baelemans A, Erlanson-Albertsson C. Effects of sucrose, glucose and fructose on peripheral and central appetite signals. Regulatory Peptides. 2008;150:26–32. doi: 10.1016/j.regpep.2008.06.008. [PubMed] [Cross Ref]
  56. Lyly M, Liukkonen KH, Salmenkallio-Marttila M, Karhunen L, Poutanen K, Lahteenmaki L, Lyly M. Fibre in beverages can enhance perceived satiety. European Journal of Nutrition. 2009;48:251–258. doi: 10.1007/s00394-009-0009-y. [PubMed] [Cross Ref]
  57. Monsivais P, Perrigue MM, Drewnowski A, Monsivais P, Perrigue MM, Drewnowski A. Sugars and satiety: does the type of sweetener make a difference? American Journal of Clinical Nutrition. 2007;86:116–123. [PubMed]
  58. Niwano Y, Adachi T, Kashimura J, Sakata T, Sasaki H, Sekine K, Yamamoto S, Yonekubo A, Kimura S, Niwano Y. et al. Is glycemic index of food a feasible predictor of appetite, hunger, and satiety? Journal of Nutritional Science & Vitaminology. 2009;55:201–207. [PubMed]
  59. Parra D, Ramel A, Bandarra N, Kiely M, Martinez JA, Thorsdottir I, Parra D, Ramel A, Bandarra N, Kiely M. et al. A diet rich in long chain omega-3 fatty acids modulates satiety in overweight and obese volunteers during weight loss. Appetite. 2008;51:676–680. doi: 10.1016/j.appet.2008.06.003.[PubMed] [Cross Ref]
  60. Rodriguez-Rodriguez E, Aparicio A, Bermejo LM, Lopez-Sobaler AM, Ortega RM. Changes in the sensation of hunger and well-being before and after meals in overweight/obese women following two types of hypoenergetic diet. Public Health Nutrition. 2009;12:44–50. doi: 10.1017/S1368980008001912. [PubMed] [Cross Ref]
  61. Sacks FM, Bray GA, Carey VJ, Smith SR, Ryan DH, Anton SD, McManus K, Champagne CM, Bishop LM, Laranjo N. et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. New England Journal of Medicine. 2009;360:859–873. doi: 10.1056/NEJMoa0804748. [PMC free article] [PubMed] [Cross Ref]
  62. Aston LM, Stokes CS, Jebb SA. No effect of a diet with a reduced glycaemic index on satiety, energy intake and body weight in overweight and obese women. International Journal of Obesity. 2008;32:160–165. doi: 10.1038/sj.ijo.0803717. [PMC free article] [PubMed] [Cross Ref]
  63. Major GC, Doucet E, Jacqmain M, St-Onge M, Bouchard C, Tremblay A, Major GC, Doucet E, Jacqmain M, St-Onge M. et al. Multivitamin and dietary supplements, body weight and appetite: results from a cross-sectional and a randomised double-blind placebo-controlled study. British Journal of Nutrition. 2008;99:1157–1167. doi: 10.1017/S0007114507853335. [PubMed] [Cross Ref]
  64. Ames BN. Micronutrients prevent cancer and delay aging. Toxicology Letters. 1998;102-103:5–18. doi: 10.1016/S0378-4274(98)00269-0. [PubMed] [Cross Ref]
  65. Astley SB, Elliott RM, Archer DB, Southon S, Astley SB, Elliott RM, Archer DB, Southon S. Increased cellular carotenoid levels reduce the persistence of DNA single-strand breaks after oxidative challenge. Nutrition & Cancer. 2002;43:202–213. [PubMed]
  66. Aviram M, Kaplan M, Rosenblat M, Fuhrman B. Dietary antioxidants and paraoxonases against LDL oxidation and atherosclerosis development. Handbook of Experimental Pharmacology. 2005. pp. 263–300. full_text. [PubMed]
  67. Collins AR, Harrington V, Drew J, Melvin R, Collins AR, Harrington V, Drew J, Melvin R. Nutritional modulation of DNA repair in a human intervention study. Carcinogenesis. 2003;24:511–515. doi: 10.1093/carcin/24.3.511. [PubMed] [Cross Ref]
  68. Ferguson LR, Philpott M, Karunasinghe N, Ferguson LR, Philpott M, Karunasinghe N. Dietary cancer and prevention using antimutagens. Toxicology. 2004;198:147–159. doi: 10.1016/j.tox.2004.01.035. [PubMed] [Cross Ref]
  69. Joseph JA, Denisova NA, Bielinski D, Fisher DR, Shukitt-Hale B. Oxidative stress protection and vulnerability in aging: putative nutritional implications for intervention. Mechanisms of Ageing & Development. 2000;116:141–153. [PubMed]
  70. Martin KR, Failla ML, Smith JC Jr. Beta-carotene and lutein protect HepG2 human liver cells against oxidant-induced damage. Journal of Nutrition. 1996;126:2098–2106. [PubMed]
  71. O’Brien NM, Carpenter R, O’Callaghan YC, O’Grady MN, Kerry JP, O’Brien NM, Carpenter R, O’Callaghan YC, O’Grady MN, Kerry JP. Modulatory effects of resveratrol, citroflavan-3-ol, and plant-derived extracts on oxidative stress in U937 cells. Journal of Medicinal Food. 2006;9:187–195. doi: 10.1089/jmf.2006.9.187. [PubMed] [Cross Ref]
  72. O’Brien NM, Woods JA, Aherne SA, O’Callaghan YC. Cytotoxicity, genotoxicity and oxidative reactions in cell-culture models: modulatory effects of phytochemicals. Biochemical Society Transactions. 2000;28:22–26. [PubMed]
  73. Prior RL, Prior RL. Fruits and vegetables in the prevention of cellular oxidative damage. American Journal of Clinical Nutrition. 2003;78:570S–578S. [PubMed]
  74. Schaefer S, Baum M, Eisenbrand G, Janzowski C, Schaefer S, Baum M, Eisenbrand G, Janzowski C. Modulation of oxidative cell damage by reconstituted mixtures of phenolic apple juice extracts in human colon cell lines. Molecular Nutrition & Food Research. 2006;50:413–417. [PubMed]
  75. Singh M, Arseneault M, Sanderson T, Murthy V, Ramassamy C, Singh M, Arseneault M, Sanderson T, Murthy V, Ramassamy C. Challenges for research on polyphenols from foods in Alzheimer’s disease: bioavailability, metabolism, and cellular and molecular mechanisms. Journal of Agricultural & Food Chemistry. 2008;56:4855–4873. [PubMed]
  76. Sudheer AR, Muthukumaran S, Devipriya N, Menon VP, Sudheer AR, Muthukumaran S, Devipriya N, Menon VP. Ellagic acid, a natural polyphenol protects rat peripheral blood lymphocytes against nicotine-induced cellular and DNA damage in vitro: with the comparison of N-acetylcysteine. Toxicology. 2007;230:11–21. doi: 10.1016/j.tox.2006.10.010. [PubMed] [Cross Ref]
  77. Tarozzi A, Hrelia S, Angeloni C, Morroni F, Biagi P, Guardigli M, Cantelli-Forti G, Hrelia P. Antioxidant effectiveness of organically and non-organically grown red oranges in cell culture systems. European Journal of Nutrition. 2006;45:152–158. doi: 10.1007/s00394-005-0575-6.[PubMed] [Cross Ref]
  78. Joel Fuhrman, Barbara Sarter, Dale Glaser, and Steve Acocella. Changing perceptions of hunger on a high nutrient density diet. Nutr J. 2010; 9: 51. Published online 2010 Nov 7. doi: 10.1186/1475-2891-9-51 [PubMed]

Health = Nutrient Intake ÷ Calories

Dr Joel Fuhrman reverses many chronic diseases – not with medications, radiotherapy or invasive surgical procedures like stents, angioplasty or gastric bands – but simply through changing his patients’ diets.

He created the Nutritarian diet, an eating plan that incorporates the latest advances in nutritional science. At the heart of this diet is the simple health equation, H=N/C.

This equation expresses the concept that your health (H) is predicted by your nutrient intake (N) divided by your calorie intake (C). His ANDI (Aggregate Nutrient Density Index) scoring system, which measures the relative nutrient density of common foods, has helped millions of people to eat an anti-cancer, anti-chronic disease diet.

The aim is to get as high a score as possible. Each food has a given value of between 0 and 1000 per calorie.

Examples

(Refer to chart below for individual food values.)

If you eat 300 calories of food with low nutritional value (let’s say 100 calories each of white pasta, cheddar cheese and olive oil), as you will see from the chart below, these would have individual ANDI values per calorie of 11, 11 and 10 respectively. Add these together and you get 32. Multiplying by 100 calories (the amount of each consumed) gives 3200. Divide this by 300 (the total number of calories) and you get a total ANDI score of 10.7.

If, however, you eat 300 calories of food with high nutritional value (let’s say 100 calories each of sweet potato, tomato and kale), these would have individual ANDI values per calorie of 181, 186 and 1000 respectively. Add these together and you get 1367. Multiplying by 100 calories (the amount of each consumed) gives 136700. Divide this by 300 and you get a total ANDI score of 455.7.

Basically, the higher the score, the healthier the food.

What does ANDI measure?

ANDI measures calcium; the carotenoids – beta carotene, alpha carotene, lutein, zeaxanthin, and lycopene; fibre; folate; glucosinolates; iron; magnesium; niacin; selenium; vitamins B1 (thiamine), B2 (riboflavin), B6, B12, C, and E; and zinc, plus the ORAC (oxygen radical absorbance capacity) score X 2. Most importantly, the ANDI scores are based on calories, not volume or weight of food, so a lower-calorie food with more nutrients scores higher than a calorie-dense food, which is why foods like iceberg lettuce and kale score high.

Have a look below and see how popular foods stack up in terms of micronutrient density per calorie. The more nutrient-dense food you consume, the more you will be satisfied with fewer calories.

So can diet really reverse diseases? And if so which diseases?

The following are some testimonials from Dr. Fuhrman’s patients. (Full TED Talk video covering the issues in this blog can be viewed below.)

Obesity, rheumatoid arthritis, hypertension, cholesterolemia.

Migraines, seasonal allergies, depression, anxiety, insomnia, menstrual pains.

Fibromyalgia, diabetes, hypertension.

Heart disease (no longer needed angioplasty), cholesterolemia, hypertension, obesity.

Psoriatic arthritis, psoriasis.

Triple vessel heart disease, (no longer needed stent replacement & angioplasty), hypertension.

[su_box title=”HIPPOCRATES” style=”glass” box_color=”#9cea59″ title_color=”#fbe42b” radius=”10″]Let food by thy medicine and let medicine be thy food.[/su_box]

G-BOMBS

Dr. Fuhrman coined the acronym G-BOMBS (Green Beans Onions Mushrooms Berries & Seeds) to represent those foods he considers are the immune system’s “special forces” – inhibiting fat storage, preventing cancer and prolonging our healthy lifespan.

I hope you are able to use this information to enjoy a diet that has food fighting for you rather than against you. After all, we are the food we eat – quite literally…

TED Talk Video

About Dr. Fuhrman

Joel Fuhrman, M.D. is a board-certified family physician, six-time New York Times best-selling author and internationally recognised expert on nutrition and natural healing.

He specialises in preventing and reversing disease through nutritional methods. He coined the term “Nutritarian” to describe his eating style, which is built around a diet of nutrient-dense, plant-rich foods.

For over 25 years, Dr. Fuhrman has shown that it is possible to achieve sustainable weight loss and reverse heart disease, diabetes and many other illnesses using smart nutrition. In his medical practice, and through his books and television specials, he continues to bring this life-saving message to hundreds of thousands of people around the world.

Dr. Fuhrman is the President of the Nutritional Research Foundation. He is also a member of the Dr. Oz Show Medical Advisory Board. He is a graduate of the University of Pennsylvania (Pearlman) School of Medicine (1988) and has received the St. Joseph’s Family Practice Resident’s Teaching Award for his contribution to the education of residents.

References

Dr. Fuhrman’s TED Talk (from which slides were taken)

Dr. Fuhrman’s ANDI scores

Dr. Fuhrman’s website

Chalkboard (more on the ANDI system)

Books:

The End of Diabetes

Super Immunity

Eat Right America

Eat For Health