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Insulin Resistance, the silent killer and root cause of modern chronic disease.

Insulin is much more than a blood sugar hormone. Produced by the pancreas primarily in response to carbohydrate and sugar consumption, insulin is a master anabolic signal that dictates how every cell in your body grows, uses energy, and repairs itself. When insulin levels are healthy, it keeps the body in a state of “build and store.” When insulin resistance (IR) develops, the body loses its ability to hear this signal, leading to systemic breakdown. Instead of “build and store” the body deteriorates, causing loss of muscle mass, strength, energy production, memory and cognitive function, bone strength, brain cells and connections, ability of blood vessels to relax, ability for the heart to pump blood, ability to achieve restorative sleep, ability of the liver and kidneys to clear toxins from the body, even the ability to reproduce resulting in infertility and erectile dysfunction. Visceral fat stores increase to destructive levels resulting in obesity and obesity-related complications including chronic inflammation which further drives IR to higher levels.

IR is a root cause of cardiovascular disease (heart attack, stroke, hypertension, heart failure), many kinds of cancer (directly linked to breast, prostate and colon cancer), kidney failure, heart failure, dementia, osteoporosis, osteoarthritis, and much more. IR is causally linked or a contributor to, every chronic non-communicable disease of modern civilization.

WHAT IS INSULIN RESISTANCE?

Insulin resistance is the inability of cells and organs to respond normally to insulin signaling. Every cell of every organ has insulin receptors that initiate action by the cell and organ.

WHAT CAUSES INSULIN RESISTANCE?

There are many causes of IR. Stress hormones (cortisol, adrenaline), inflammation, and high insulin levels themselves (response to dietary sugar and refined carbohydrates), each alone and in combination, cause immediate (within minutes to hours) insulin resistance. When these conditions persist over time insulin resistance becomes a chronic state. As fat cells grow in size, they reach a point where there is inadequate blood flow to the cells themselves and macrophages (immune cells that reside between the fat cells, most prominently in visceral fat) produce inflammatory chemicals called cytokines. Cytokines flow through the blood stream and effect every organ and every cell in the body creating a state of chronic inflammation which further worsens IR, creating a vicious cycle. As IR continues the pancreas produces increasingly higher amounts of insulin to maintain normal blood sugar levels but eventually IR becomes so great that blood sugar levels move into the “pre-diabetes” and eventually the diabetes range. IR builds for years to decades before blood sugar regulation fails. By the time blood sugar levels are “abnormal” insulin resistance has done great damage throughout the body.

Most doctors tragically do not order fasting insulin levels as routine blood tests. Fasting insulin levels rise long before fasting blood sugars and hemoglobin A1c start to rise. Meanwhile the damage progresses under the radar of routine testing.

1. Metabolic Engines: Muscle and Liver

Muscle

Normal Action: Insulin acts as a key that opens “doors” (GLUT4 receptors) to let glucose in for fuel. it also stimulates protein synthesis. Protein synthesis is essential to maintaining and increasing muscle mass and strength.
Insulin Resistance Effect: The “doors” stay locked. Glucose stays in the blood, and the muscle becomes “starched,” leading to sarcopenia (muscle wasting) and fatigue. The muscle can no longer utilize dietary protein to maintain or increase muscle mass.

Liver

Normal Action: Tells the liver to stop producing glucose and start storing it as glycogen or converting excess into fat.
Insulin Resistance Effect: The liver ignores the “stop” signal and keeps pumping out glucose while simultaneously ramping up fat production. This results in Non-Alcoholic Fatty Liver Disease (NAFLD).

2. Fat Cells (Adipose Tissue)

Visceral (Deep Fat) vs. Subcutaneous (Under Skin)

Normal Action: Insulin promotes fat storage and inhibits the breakdown of stored fat (lipolysis).
Insulin Resistance Effect: Fat cells—especially visceral ones—become “leaky.” They spill free fatty acids into the bloodstream and release inflammatory cytokines. This causes weight gain that is biologically difficult to lose because high insulin levels keep the “fat-burning” switch permanently off.

3. The Vital Organs: Heart, Kidneys, and Arteries

Heart and Arteries

Normal Action: Insulin stimulates the release of nitric oxide, which helps arteries relax and dilate.
Insulin Resistance Effect: Nitric oxide production drops, causing arteries to stiffen (hypertension). High insulin also damages the endothelial lining, leading to atherosclerosis (plaque buildup). This is the primary driver of heart failure, heart attacks and strokes.

Kidneys

Normal Action: Helps regulate sodium reabsorption.
Insulin Resistance Effect: The kidneys hold onto too much salt, increasing blood pressure. Over time, high blood sugar and inflammation damage the filtering units, leading to chronic kidney disease (CKD).

4. The Brain, Memory, and Sleep

Brain and Memory

Normal Action: Insulin crosses the blood-brain barrier to regulate appetite and support synaptic plasticity (the basis of learning).
Insulin Resistance Effect: Often called “Type 3 Diabetes,” brain IR starves neurons of energy and allows amyloid plaques and neurofibrillary tangles to build up. Worse, the brain is unable to utilize glucose to meet energy demands it starts to malfunction. This is a direct pathway to Alzheimer’s disease and dementia. As the small arteries in the brain become atherosclerotic and unable to deliver adequate oxygen and nourishment to brain cells small areas of the brain become permanently damaged eventually leading to vascular dementia.

Sleep

Insulin Resistance Effect: IR is heavily linked to Obstructive Sleep Apnea. (OSA) High insulin affects the central respiratory drive and increases fat deposits around the neck (a major contributor to obstructive sleep apnea), disrupting sleep cycles and creating periods of inadequate oxygen flow to the brain resulting in the acute stress response and awakening with each apneic event. Even without OSA, high insulin levels impair the production of melatonin which is essential to normal-restorative sleep. Throughout the day the brain accumulates metabolic toxins that must be cleared through the glymphatic system at night during sleep. As sleep is impaired this clearance system is disrupted, contributing to structural damage and functional loss. Sleep disruption and apneic episodes are stressful events, increasing stress hormones which then worsen IR, creating another vicious cycle. One night of sleep disruption causes acute IR. Chronic sleep disruption contributes to chronic IR.

5. Immunity and Structural Health

Immune System

Action: High insulin/glucose impairs white blood cell function.
Effect: Chronic inflammation (high CRP levels) and a weakened defense against infections. This is why diabetics often have poor wound healing. As normal immune regulation is impaired the immune system both over-reacts and under-reacts. Under-reaction increases risk of infection. Over-reaction produces cytokine storms seen with Covid-19 and other infections. Chronic inflammation worsens IR creating another vicious cycle. Chronic inflammation contributes to most chronic diseases.

Bone and Joints

Action: Insulin is bone-building.
Effect: IR leads to poor bone quality (despite high density) and osteoarthritis due to systemic inflammation and the “glycosylation” (sugar-coating) of joint cartilage, making it brittle.

6. The Pancreas: Beta and Alpha Cells

Normal Action: Beta cells produce insulin; Alpha cells produce glucagon (which raises sugar). They balance each other.
Insulin Resistance Effect:
- Beta Cells: Work overtime to produce massive amounts of insulin to compensate, eventually “burning out” and dying. This can produce per4manent irreversible damage to the pancreas.
- Alpha Cells: Become resistant to insulin’s “stop” signal and keep secreting glucagon, further raising blood sugar levels which in turn cause higher insulin secretion, both of which worsen IR, creating another vicious cycle.

7. Reproductive Effects: Infertility

In Women: High insulin stimulates the ovaries to produce excess testosterone, which is the primary driver of Polycystic Ovary Syndrome (PCOS) and infertility.
In Men: IR is a leading cause of low testosterone and erectile dysfunction (due to the arterial damage mentioned above).

Summary of Systemic Effects

Condition	Primary Mechanism of Insulin Resistance
Atherosclerosis	Endothelial dysfunction, high triglycerides, low HDL, increased TG/HDL ratio, increased small dense LDL and remnant particles, increased endothelial permeability.
Dementia	Neuronal glucose starvation and plaque buildup, brain small vessel disease, disruption of blood brain barrier.
Chronic Inflammation	Release of cytokines from visceral fat.
Heart Failure	Stiffening of the heart muscle and high blood pressure.
Diabetes	Pancreatic beta cell and alpha cell damage

Insulin’s Role vs. Insulin Resistance (IR)

Organ/System	Normal Insulin Action	Effects of Insulin Resistance
Liver	Stops glucose production; stores glucose as glycogen.	The liver ignores the “stop” signal, pumping out sugar even when you haven’t eaten (fatty liver).Fatty liver disease is the greatest cause of liver failure in the US.
Muscle	Primary site for glucose uptake; promotes protein synthesis.	Muscles can’t take in fuel efficiently, leading to fatigue and muscle wasting (sarcopenia). Muscle cells cannot use amino acids from dietary protein to maintain or build muscle. Elderly lose muscle and strength, resulting in falls, fractures and head trauma. Loss of muscle (the major sink for blood sugar after a meal) further increases duration and degree of blood sugar and insulin rise after a meal, which in turn increases IR. (vicious cycle)
Fat (Adipose)	Stores fat; inhibits the breakdown of stored fat.	Fat cells leak fatty acids into the blood, leading to high triglycerides and visceral fat gain. Macrophages (immune cells) produce inflammatory cytokines which circulate through the body contributing to chronic inflammation which worsens IR, another vicious cycle.
Brain	Regulates appetite, memory, and cognitive function.	Linked to “Type 3 Diabetes”; impaired memory and increased risk of neurodegeneration. Brain loses ability to meet energy demands and clear toxins. Insulin resistance in the brain explains memory loss, cognitive impairment, loss of neurons and synapses, loss of neuroplasticity. BDNF (brain derived neurotrophic factor) production is decreased by IR.
Arteries	Stimulates nitric oxide for vasodilation (keeps vessels flexible).	Reduced nitric oxide causes vessels to stiffen, raising blood pressure and plaque buildup. This is called endothelial dysfunction, the precursor to heart attack, stroke, peripheral vascular disease and a root cause for neuropathy and amputations.
Heart	Regulates fuel use (switching between glucose and fats).	The heart becomes “metabolically inflexible,” increasing the risk of heart failure.
Kidney	Manages sodium reabsorption and filtration.	High insulin causes the kidneys to hold onto salt, driving up blood pressure and damaging filters. Oxidative stress leads to kidney failure.
Immune System	Modulates inflammation and helps T-cell function.	Creates a state of “chronic low-grade inflammation” and weakens the response to infections.
Bone	Stimulates bone-forming cells (osteoblasts).	Bone quality decreases; despite higher bone density in some cases, the bones are more brittle.
Joints	Maintains cartilage and reduces systemic inflammation.	High insulin promotes pro-inflammatory cytokines, accelerating osteoarthritis and gout.

A meal with sugar and refined carbohydrates causes excessive swings in blood sugar and insulin levels, creating insulin resistance and downstream damage. Alcohol consumption contributes to this process. Fat consumption does not cause a rise in blood sugar or insulin levels. Protein consumption produces a minimal rise in insulin levels in the absence of IR.

Fat storage can occur through hyperplasia (increase in number of fat cells) or hypertrophy (increase in size). Some ethnic groups are more prone to hypertrophy (south and east Asian). Hypertrophy in visceral fat (fat around the internal organs as opposed to fat under the skin) results in macrophage production of inflammatory cytokines. Eventually, the fat cells themselves can literally burst from too much volume.

In my next post, I will discuss what we can do to prevent and reverse IR.

REFERENCES

Chadt A, Al-Hasani H. Glucose transporters in adipose tissue, liver, and skeletal muscle in metabolic health and disease. Pflugers Arch. 2020 Sep;472(9):1273-1298. doi: 10.1007/s00424-020-02417-x. Epub 2020 Jun 26. PMID: 32591906; PMCID: PMC7462924.

https://pmc.ncbi.nlm.nih.gov/articles/PMC7462924/

Fujita S, Rasmussen BB, Cadenas JG, Grady JJ, Volpi E. Effect of insulin on human skeletal muscle protein synthesis is modulated by insulin-induced changes in muscle blood flow and amino acid availability. Am J Physiol Endocrinol Metab. 2006 Oct;291(4):E745-54. doi: 10.1152/ajpendo.00271.2005. Epub 2006 May 16. PMID: 16705054; PMCID: PMC2804964.

https://pmc.ncbi.nlm.nih.gov/articles/PMC2804964

Vargas E, Joy NV, Carrillo Sepulveda MA. Biochemistry, Insulin Metabolic Effects. [Updated 2022 Sep 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK525983/

https://www.ncbi.nlm.nih.gov/books/NBK525983/

Bugianesi E, Moscatiello S, Ciaravella MF, Marchesini G. Insulin resistance in nonalcoholic fatty liver disease. Curr Pharm Des. 2010 Jun;16(17):1941-51. doi: 10.2174/138161210791208875. PMID: 20370677.

https://pubmed.ncbi.nlm.nih.gov/20370677/

Cardillo C, Nambi SS, Kilcoyne CM, Choucair WK, Katz A, Quon MJ, Panza JA. Insulin stimulates both endothelin and nitric oxide activity in the human forearm. Circulation. 1999 Aug 24;100(8):820-5. doi: 10.1161/01.cir.100.8.820. PMID: 10458717.

https://pubmed.ncbi.nlm.nih.gov/10458717/

Ke JF, Wang JW, Zhang ZH, Chen MY, Lu JX, Li LX. Insulin Therapy Is Associated With an Increased Risk of Carotid Plaque in Type 2 Diabetes: A Real-World Study. Front Cardiovasc Med. 2021 Feb 1;8:599545. doi: 10.3389/fcvm.2021.599545. PMID: 33598483; PMCID: PMC7882504.

https://pubmed.ncbi.nlm.nih.gov/33598483/

Brosolo G, Da Porto A, Bulfone L, Vacca A, Bertin N, Scandolin L, Catena C, Sechi LA. Insulin Resistance and High Blood Pressure: Mechanistic Insight on the Role of the Kidney. Biomedicines. 2022 Sep 23;10(10):2374. doi: 10.3390/biomedicines10102374. PMID: 36289636; PMCID: PMC9598512.

https://pubmed.ncbi.nlm.nih.gov/36289636/

Kumar M, Dev S, Khalid MU, Siddenthi SM, Noman M, John C, Akubuiro C, Haider A, Rani R, Kashif M, Varrassi G, Khatri M, Kumar S, Mohamad T. The Bidirectional Link Between Diabetes and Kidney Disease: Mechanisms and Management. Cureus. 2023 Sep 20;15(9):e45615. doi: 10.7759/cureus.45615. PMID: 37868469; PMCID: PMC10588295.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10588295/

Banks WA, Owen JB, Erickson MA. Insulin in the brain: there and back again. Pharmacol Ther. 2012 Oct;136(1):82-93. doi: 10.1016/j.pharmthera.2012.07.006. Epub 2012 Jul 17. PMID: 22820012; PMCID: PMC4134675.

https://pubmed.ncbi.nlm.nih.gov/22820012/

Rahman MS, Hossain KS, Das S, Kundu S, Adegoke EO, Rahman MA, Hannan MA, Uddin MJ, Pang MG. Role of Insulin in Health and Disease: An Update. Int J Mol Sci. 2021 Jun 15;22(12):6403. doi: 10.3390/ijms22126403. PMID: 34203830; PMCID: PMC8232639.

https://pmc.ncbi.nlm.nih.gov/articles/PMC8232639/

Scherrer U, Sartori C. Insulin as a vascular and sympathoexcitatory hormone: implications for blood pressure regulation, insulin sensitivity, and cardiovascular morbidity. Circulation. 1997 Dec 2;96(11):4104-13. doi: 10.1161/01.cir.96.11.4104. PMID: 9403636.

https://pubmed.ncbi.nlm.nih.gov/9403636/

Affuso F, Micillo F, Fazio S. Insulin Resistance, a Risk Factor for Alzheimer’s Disease: Pathological Mechanisms and a New Proposal for a Preventive Therapeutic Approach. Biomedicines. 2024 Aug 19;12(8):1888. doi: 10.3390/biomedicines12081888. PMID: 39200352; PMCID: PMC11351221.

https://pmc.ncbi.nlm.nih.gov/articles/PMC11351221/

Park MH, Kim DH, Lee EK, Kim ND, Im DS, Lee J, Yu BP, Chung HY. Age-related inflammation and insulin resistance: a review of their intricate interdependency. Arch Pharm Res. 2014 Dec;37(12):1507-14. doi: 10.1007/s12272-014-0474-6. Epub 2014 Sep 20. PMID: 25239110; PMCID: PMC4246128.

https://pubmed.ncbi.nlm.nih.gov/25239110/

Hardy OT, Czech MP, Corvera S. What causes the insulin resistance underlying obesity? Curr Opin Endocrinol Diabetes Obes. 2012 Apr;19(2):81-7. doi: 10.1097/MED.0b013e3283514e13. PMID: 22327367; PMCID: PMC4038351.

https://pmc.ncbi.nlm.nih.gov/articles/PMC4038351/

THIS WEBSITE PROVIDES INFORMATION FOR EDUCATIONAL PURPOSES ONLY. CONSULT YOUR HEALTH CARE PROVIDER FOR MEDICAL ADVICE.

Eat clean, drink filtered water, love, laugh, exercise outdoors in a greenspace, get some morning sunlight, block the blue light before bed, engage in meaningful work, find a sense of purpose, spend time with those you love, AND sleep well tonight.

Doctor Bob

The new dietary guidelines, a major improvement

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The new Dietary Guidelines for Americans (DGA) represent a major improvement over previous guidelines. The storm of criticism registered by some “experts” and quoted by the media is NOT based on valid evidence. There has been excessive and irrational criticism over inverting the food pyramid, with animal sources of protein on the top. Until now recommendations for daily protein intake have been based upon estimates to avoid protein deficiency rather than optimization. The recommendations for 1.2-1.6 grams per kilogram bodyweight per day (up from 0.8 g/kg/day) is supported by data on muscle building, muscle maintenance and bone health (when combined with resistance exercise), especially for elderly individuals.

Unfortunately, the 10% restriction on saturated fat remains, but the guidelines appropriately state that there is a lack of evidence to keep that restriction at 10% of caloric intake. The controversy over saturated fat remains despite meta-analyses of randomized controlled clinical trials that conclude that restriction of saturated fat has not been found to improve cardiovascular, metabolic, or cancer outcomes.

I doubt that those critical of the new DGA have read the 416-page appendices that document scientific references and explanations for each of the dietary recommendations. That’s right, 416 pages of narrative and scientific references are in the appendices of the DGA.

If you go here, you can download 4 documents including the Scientific Foundation Appendices (416 pages), the Scientific Foundation for DGA (90 pages), The Daily Servings Guide (3 pages) and the DGA (10 pages)

Here is an excerpt that is very useful.

How can you identify highly processed foods? Highly processed foods tend to have: 1. Refined grains and/or added sugars 2. Refined fats and oils 3. Long, complicated ingredient lists including chemical additives (e.g., artificial sweeteners, flavor enhancers, artificial colors, and emulsifiers). Examples are provided in Figures 4.3 and 5.8.

And a good explanation for why refined grains (any food made with flour) causes rapid and high blood sugar responses.

Refined Grains and Starches are Sugar • Refined grains are highly purified sources of starch. • Starches are long chains of glucose—a form of sugar. • During chewing and digestion, enzymes rapidly break down starch into glucose, raising blood sugar much like table sugar does. • Refined grain foods—white bread, crackers, breakfast cereals, chips, pastries, and pasta—can therefore act metabolically like sugar, delivering fast-absorbing carbohydrates with few nutrients or fiber to slow absorption. Take-home message: Refined grains are sugar in disguise. Choose whole grains, beans, or vegetables instead.

The following two graphics demonstrate the results of previous dietary guidelines that demonized healthy fats and animal sources of protein. The first shows the rise in obesity and diabetes but does not address the insulin resistance that evolves over decades before crossing the arbitrary threshold of diabetes, wreaking metabolic havoc long before diabetes occurs. The second graphic reveals how Americans consume 60% or more caloric intake in the form of refined carbohydrates (equivalent to sugar)

The following graphic displays the difference between minimally processed, moderately processed and highly processed foods according to the NOVA classification system (a system I will discuss and criticize in future posts). For now, suffice it to say that a simpler and more practical definition of “processed food” would include any food with one or more of the following: added sugar, artificial sweeteners, refined starch especially flour made from grains, refined “vegetable” oils, emulsifiers, artificial coloring, preservatives, and other additives found to disrupt the microbiome, intestinal barrier function or cause cancer. This graphic importantly covers the issue of food packaging which can contribute to the consumption of micro plastics, phthalates and PFAs

I have consistently advocated for a diet that consists of free-range meat, poultry, eggs, seafood (low mercury varieties), organic vegetables, fruits, nuts, seeds, an ancestral or paleo diet. The new DGA go a long way to produce evidence-based recommendations to help Americans eat healthy food. I continue to advocate for getting fiber from vegetables and fruits, eliminating grains, for reasons previously discussed but if you want to eat grains and are not gluten sensitive or suffer from celiac disease, consume the grains as a whole food, not in a food made from flour. “Whole grain bread” is not a whole grain food, nor is “whole grain” pasta. Once flour is made from grains the cellular components are destroyed producing a product with a glycemic index akin to sugar with the resultant metabolic disturbance which over the long run leads to insulin resistance, obesity and chronic disease.

If you want to consume dairy it makes much more sense to consume full fat fermented dairy foods instead of the low-fat dairy products advocated by prior DGA. The new DGA go into great detail to describe the nutrient deficiencies associated with vegan and vegetarian diets unless specific supplements are consumed. Specific recommendations for pregnant and breast-feeding mothers cover most important points as do age specific recommendations for infants and children. The importance of choline could have received a little more attention (best sources include eggs and liver). The importance of marine omega-3 fats (EPA, DHA, DPA) received adequate attention.

Overall, I consider the 2026 DGA a major improvement compared to previous iterations which ignored a large body of nutritional science.

The following references support my position on SFA and properly raised and prepared animal protein.

https://pubmed.ncbi.nlm.nih.gov/32562735/

Astrup A, Magkos F, Bier DM, Brenna JT, de Oliveira Otto MC, Hill JO, King JC, Mente A, Ordovas JM, Volek JS, Yusuf S, Krauss RM. Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020 Aug 18;76(7):844-857. doi: 10.1016/j.jacc.2020.05.077. Epub 2020 Jun 17. PMID: 32562735.

Reimara Valk, James Hammill, Jonas Grip, Saturated fat: villain and bogeyman in the development of cardiovascular disease?, European Journal of Preventive Cardiology, Volume 29, Issue 18, December 2022, Pages 2312–2321, https://doi.org/10.1093/eurjpc/zwac194

Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study Dehghan, MahshidDiaz, R et al. The Lancet, Volume 390, Issue 10107, 2050 – 2062

https://pubmed.ncbi.nlm.nih.gov/36216940/

Lescinsky H, Afshin A, Ashbaugh C, Bisignano C, Brauer M, Ferrara G, Hay SI, He J, Iannucci V, Marczak LB, McLaughlin SA, Mullany EC, Parent MC, Serfes AL, Sorensen RJD, Aravkin AY, Zheng P, Murray CJL. Health effects associated with consumption of unprocessed red meat: a Burden of Proof study. Nat Med. 2022 Oct;28(10):2075-2082. doi: 10.1038/s41591-022-01968-z. Epub 2022 Oct 10. PMID: 36216940; PMCID: PMC9556326.

Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis Renata Micha ¹, Sarah K Wallace, Dariush Mozaffarian, Circulation CIRCULATIONAHA.109.924977. Epub 2010 May 17. https://pubmed.ncbi.nlm.nih.gov/20479151/

Unprocessed Red Meat and Processed Meat Consumption: Dietary Guideline Recommendations from the Nutritional Recommendations (NutriRECS) Consortium Bradley C. Johnston, PhD, Dena Zeraatkar, Msc, et. al. Ann Intern Med 2019: 1:756-764 doi: 10.7326/M19-1621

Reduction of Red and Processed Meat Intake and Cancer Mortality and Incidence A Systematic Review and Meta-analysis of Cohort Studies Mi Ah Han, MD, PhD; Dena Zeraatkar, MSc; et. al., Ann Intern Med. 2019;171:711-720. doi:10.7326/M19-0699

Patterns of Red and Processed Meat Consumption and Risk for Cardiometabolic and Cancer Outcomes A Systematic Review and Meta-analysis of Cohort Studies Robin W.M. Vernooij, PhD*; Dena Zeraatkar, MSc Ann Intern Med.2019;171:732-741. doi:10.7326/M19-1583

Red and Processed Meat Consumption and Risk for All-Cause Mortality and Cardiometabolic OutcomesA Systematic Review and Meta-analysis of Cohort Studies Dena Zeraatkar, MSc, Mi Ah Han MD, PhD, et. al, Annals of Internal Medicine 1 October 2019: 171-710 doi: 10.7326/M19-0655

Effect of Lower Versus Higher Red Meat Intake on Cardiometabolic and Cancer Outcomes

A Systematic Review of Randomized Trials Dena Zeraatkar, MSc, Bradley C Johnston, PhD, et. al. Ann Intern Med. 2019;171:721-731. doi:10.7326/M19-https://doi.org/10.7326/M19-0622

E, Lavie CJ, Hill JO. The Failure to Measure Dietary Intake Engendered a Fictional Discourse on Diet-Disease Relations. Front Nutr. 2018 Nov 13;5:105. doi: 10.3389/fnut.2018.00105. PMID: 30483510 Archer; PMCID: PMC6243202.

Archer E, Hand GA, Blair SN (2013) Validity of U.S. Nutritional Surveillance: National Health and Nutrition Examination Survey Caloric Energy Intake Data, 1971–2010. PLoS ONE 8(10): e76632. https://doi.org/10.1371/journal.pone.0076632

O’Connor, Lauren E., et al. “Effects of total red meat intake on glycemic control and inflammatory biomarkers: a meta-analysis of randomized controlled trials.” Advances in Nutrition 12.1 (2021): 115-127.

Kiani AK, Dhuli K, Donato K, Aquilanti B, Velluti V, Matera G, Iaconelli A, Connelly ST, Bellinato F, Gisondi P, Bertelli M. Main nutritional deficiencies. J Prev Med Hyg 2022;63(suppl.3):E93-E101.https://doi.org/10.15167/2421-4248/jpmh2022.63.2S3.2752

Bailey RL, West KP Jr, Black RE. The epidemiology of global micronutrient deficiencies. Ann Nutr Metab. 2015;66 Suppl 2:22-33. doi: 10.1159/000371618. Epub 2015 Jun 2. PMID: 26045325.

Global, regional and national burdens of common micronutrient deficiencies from 1990 to 2019: A secondary trend analysis based on the Global Burden of Disease 2019 study. Zu Han et. al., eClinicalMedicine, February 11, 2022 https://doi.org/10.1016/j.eclinm.2022.101299

Sean R. Lynch, Why Nutritional Iron Deficiency Persists as a Worldwide Problem, The Journal of Nutrition, Volume 141, Issue 4, April 2011, Pages 763S–768S, https://doi.org/10.3945/jn.110.130609

Meat supplementation improves growth, cognitive, and behavioral outcomes in Kenyan children , J Nutr. 2007 Apr;137(4):1119-23.

Animal source foods have a positive impact on the primary school test scores of Kenyan schoolchildren in a cluster-randomised, controlled feeding intervention trial – PubMed (nih.gov), Hulett JL, Weiss RE, Bwibo NO, Galal OM, Drorbaugh N, Neumann CG.Br J Nutr. 2014 Mar 14;111(5):875-86. doi: 10.1017/S0007114513003310. Epub 2013 Oct 30.PMID: 24168874 Clinical Trial.

Meat supplementation increases arm muscle area in Kenyan schoolchildren – PubMed (nih.gov), Br J Nutr. 2013 Apr 14;109(7):1230-40. doi: 10.1017/S0007114512003121. Epub 2012 Aug 2.PMID: 22856533 Clinical Trial.

School snacks decrease morbidity in Kenyan schoolchildren: a cluster randomized, controlled feeding intervention trial.

Neumann CG, Bwibo NO, Jiang L, Weiss RE.Public Health Nutr. 2013 Sep;16(9):1593-604. doi: 10.1017/S1368980013000876. Epub 2013 Mar 28.PMID: 23537728

Effects of animal source foods, with emphasis on milk, in the diet of children in low-income countries.

Allen LH, Dror DK.Nestle Nutr Workshop Ser Pediatr Program. 2011;67:113-30. doi: 10.1159/000325579. Epub 2011 Feb 16.PMID: 21335994

https://www.bmj.com/content/351/bmj.h4962

The scientific report guiding the US dietary guidelines: is it scientific?

BMJ 2015; 351 doi: https://doi.org/10.1136/bmj.h4962 (Published 23 September 2015)

https://pmc.ncbi.nlm.nih.gov/articles/PMC9794145/

Teicholz N. A short history of saturated fat: the making and unmaking of a scientific consensus. Curr Opin Endocrinol Diabetes Obes. 2023 Feb 1;30(1):65-71. doi: 10.1097/MED.0000000000000791. Epub 2022 Dec 8. Erratum in: Curr Opin Endocrinol Diabetes Obes. 2025 Aug 1;32(4):166. doi: 10.1097/01.med.0001118356.22843.75. PMID: 36477384; PMCID: PMC9794145.

THIS WEBSITE PROVIDES INFORMATION FOR EDUCATIONAL PURPOSES ONLY. CONSULT YOUR HEALTH CARE PROVIDER FOR MEDICAL ADVICE.

Doctor Bob

Omega-3 fatty acids, Pain and Arthritis

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Before modern pharmacy an early treatment for Rheumatoid Arthritis (RA) was cod liver oil, rich in omega-3 fats and vitamin D. A 2013 study demonstrated that consumption of cod liver oil resulted in a reduction of daily diclofenac in Rheumatoid Arthritis. As early as 1959 cod liver oil was recommended for arthritis in the medical literature. A 2017 review of marine omega-3 fats for arthritis pain found moderate quality evidence in rheumatoid arthritis patients. A 2024 review of prevention and treatment for RA suggested that a diet rich in fiber, vitamins, omega 3 and low glycemic index foods contributes to protection from RA. A comprehensive review of omega-3 fatty acids for RA included analysis of several studies and concluded that omega-3 was a valuable therapeutic option to improve pain symptoms, tender joint count, duration of morning stiffness and the frequency of NSAID consumption. A 2019 review of cumulative data on omega-3 fats to combat autoimmune diseases concluded:

“The promising findings coming from the cumulative research work over the last decade solidified the role of ω-3 PUFAs as a potential candidate to prevent or even treat such autoimmune diseases as type 1 diabetes, RA, SLE, MS”

A 2024 review of marine omega-3 PUFA (polyunsaturated fatty acids) for RA reported:

“Altogether the data reported in this review show that anti-inflammatory interventions, i.e., high fish consumption or supplements containing n-3 PUFAs, should be the standard of care, along with pharmacotherapy, in treating patients with RA.”

And here is a graphic from that article showing the effect of SPMs (specialized pro-resolving mediators, derived from omega-3s):

What about osteoarthritis?

A multicenter randomized double blind placebo controlled trial of krill oil containing 0.60 g EPA/d, 0.28 g DHA/d, 0.45 g astaxanthin/d demonstrated improvements in pain, stiffness and physical function.

Some omega-3 supplement studies have demonstrated no significant pain relief in osteoarthritis. Those studies did not reduce the consumption of pro-inflammatory n-6 fatty acids which compete with omega-3 fats for the enzymes which can lead to pro or anti-inflammatory mediators. They also did not measure the omega 6/omega 3 ratio in blood or tissues. Nor did they measure the omega-3 index (% of omega-3 achieved in red blood cell membranes, the gold standard for evaluating tissue levels achieved) This 2018 analysis stated:

“High Omega-3 (n-3) polyunsaturated fatty acids (PUFAs) are associated with lower levels of inflammatory mediators, anti-nociception, and adaptive cognitive/emotional functioning. High Omega-6 (n-6) PUFAs are associated with inflammation, nociception, and psychological distress. While findings related to n-3 supplementation in knee OA are mixed, consideration of the n-6:n-3 ratio and additional outcome measures may provide improved understanding of the potential relevance of these fatty acids in OA”

The authors went on to access blood n-6/n-3 ratios in patients with OA and found the following:

“The high ratio group reported greater pain and functional limitations, (all p’s<0.04), mechanical temporal summation (hand and knee, p<0.05), and perceived stress (p=0.008) but not depressive symptoms.”

“In adults with knee pain, a high n-6:n-3 ratio is associated with greater clinical pain/functional limitations, experimental pain sensitivity, and psychosocial distress compared to a low ratio group.”

The anti-inflammatory diet that I follow and recommend eliminates the major sources of excess omega-6 in the diet, specifically the “vegetable oils” which are actually seed, grain, and legume oils predominated by soy oil, corn oil, peanut and cottonseed oil present in cooking “vegetable oils” and processed foods. A table that displays the ratio of omega 3 to omega 6 in various oils can be found here. Note that this table does not reveal the amounts of MUFA (mono unsaturated fatty acids) which are arguably “heart healthy”. Nor does it address the important issue of protective polyphenols and anti-oxidants (such as in Extra Virgin Olive oil aka EVOO). So do not make choices of oil based only on the omega-3/6 ratio.

Another consideration in choosing oils for cooking (as opposed to salad dressing) is the smoke point. Under high heat, oils are subject to oxidation which creates a proinflammatory effect when consumed. Refined Avocado oil has the highest smoke point (520 degrees F). But we digress. Back to pain and arthritis.

An article just published in Nutrients reviewed Omega-3 Supplementation and Its Effects on Osteoarthritis.

“omega-3 polyunsaturated fatty acids (PUFA) have demonstrated an influential role in the progression of OA, resulting in the reduction of cartilage destruction, inhibition of pro-inflammatory cytokine cascades, and production of oxylipins that promote anti-inflammatory pathways.”

“Research has demonstrated a positive effect on the modulation of OA symptoms through diet and exercise to promote an anti-inflammatory environment. More specifically, omega-3 PUFAs have demonstrated a reduction in inflammatory biomarkers and cartilage degradation, counteracting the natural disease state of OA. In addition to their chondroprotective role, omega-3 supplementation has been shown to have indirect positive effects on muscle tissue recovery following exercise, which is necessary to prevent the progression of OA and maintain an independent, healthy lifestyle. The effects of omega-3 supplementation on the disease state of OA and its symptoms remain inconclusive. Further clinical trials utilizing human participants are warranted to provide a conclusive recommendation on standardized supplementation of omega-3 for the modulation of osteoarthritis.”

Given the cardioprotective effects, discussed in my last post (including an 80% reduction in sudden death at the highest quintile of omega-3 index) and other benefits (reduction in all cause mortality with high tissue levels), there are many reasons to include large amounts of low mercury fatty fish (wild Alaskan salmon, sardines, herring, trout) in the diet and to consider supplementation when your omega 3 index is < 8%. Likewise, in the presence of arthritis and pain, getting tissue levels of omega 3 up and reducing excessive pro-inflammatory omega 6 will likely provide significant benefit.

Here is a graphic with the omega 3 content of some foods.

And another:

As mentioned in my previous post about omega-3 and cardiovascular health, 1800 mg of omega-3 FA daily is adequate in most people to achieve and omega-3 index of 8%, the level at which cardiovascular protection is greatest.

THIS WEBSITE PROVIDES INFORMATION FOR EDUCATIONAL PURPOSES ONLY. CONSULT YOUR HEALTH CARE PROVIDER FOR MEDICAL ADVICE.

Doctor Bob

Omega-3 in your diet and supplements

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The benefit of omega-3 supplementation has been debated in the cardiology and nutritional literature for many years. Most studies of supplementation have failed to measure tissue levels achieved and often used very low doses. But when tissue levels were measured, either in the serum or red blood cell membrane, the studies consistently demonstrated significant reductions in all-cause mortality and cardiovascular mortality associated with high levels of omega-3 fatty acids.

In addition, higher levels of omega 3 are associated with >=80% reduction in sudden death associated with acute myocardial infarction (acute MI) and > 80% reduction in sudden death in cohorts without known coronary artery disease followed long term.

Two Coronary CT Angiogram (CCTA) studies demonstrated that patients with stable coronary artery disease on statin therapy randomized to high dose EPA and DHA had “prevention of coronary plaque progression when an omega-3 fatty acid index >= 4% was achieved.”

Another CCTA study demonstrated that patients receiving omega 3 supplementation had significantly less coronary atherosclerotic “high risk” lipid rich plaque prevalence (3.8% versus 32%) and lower total non-calcified plaque burden independent of cardiovascular risk factors compared to matched controls not receiving omega 3 supplements.

Omega 3 supplementation after an acute myocardial infarction has been found to reduce infarct size, reduce scaring (fibrosis), and enhance heart tissue healing. (Randomized controlled clinical trial) However a post MI study in 1027 elderly patients randomized to receive 1.8 grams per day of EPA+DHA versus a control group receiving corn oil showed no reduction in the primary composite cardiovascular endpoint between the two groups at 2 years but a higher incidence of AF in the omega 3 group that did not reach statistical significance.

Recently a study, widely reported by the lay press, suggested that high dose omega-3 supplementation was associated with increased risk of atrial fibrillation (AF). These results conflicted with previous studies which demonstrated just the opposite, specifically prior studies demonstrated reduced risk of AF. The more recent study suffered a significant design flaw. The study in question failed to make statistical adjustment for the increased life span associated with higher levels of omega-3. Since age is a primary risk factor for AF, any intervention which increases life span would be expected to result in more AF over the lifetime of the patients as they aged (i.e., more elder years results in increased risk of AF). Therefore, statistical adjustment for that effect should be employed, but was not done in the study.

Unfortunately, science journalism has deteriorated to a state where the conclusions of study authors are most often quoted without interpretation or context, and without critical analysis or comparisons with previous studies that may have demonstrated opposing results.

In addition to large well-designed studies that have suggested a reduced risk of AF associated with omega-3 fatty acids, there have been natural experiments that provide reassuring information. The indigenous Inuit people of Greenland, for example, historically consumed large amounts of omega-3 in their diet with no evidence of increased risk of AF. In fact, before the introduction of western processed foods, estimates of AF among the Inuit were 0.6% (1963) compared to a “worldwide prevalence of AF in adults between 2 and 4%, between one and two percent in Canadian and the general US population and between 0.5% and 3% in most low- and middle-income countries.” A more recent study of Greenland yielded a prevalence of 1.4% likely reflecting a change in habits consisting of less exercise, more tobacco use and a shift to a more Western diet.

Still, multiple studies that used high dose omega 3 supplements in patients with known cardiac disease suggest an increased risk of AF. A good review of omega-3 fatty acids and atrial fibrillation was published in the Korean Journal of Internal Medicine, referenced below.

My interpretation of the complex data in this area is as follows.

At supplemental doses of EPA+DHA above 1.8 grams per day (and perhaps above 1 gram per day) in patients with known coronary artery disease (CAD), at high risk of CAD, or following a myocardial infarction, the risk of AF is increased by about 25% (relative risk). But the risk of lethal ventricular arrythmias (sudden death) associated with myocardial infarction (heart attack) is 80% lower in patients with a red blood cell omega 3 index of >=8. In people without known CAD, an omega-3 index >=8% is associated with an 80% reduction in sudden cardiac death. CCTA studies show significantly lower unstable “vulnerable” plaque in patients on omega-3 supplements. Similarly, omega 3 supplementation in patients on statins associates with halted plaque progression determined by serial CCTA in non-diabetics.

In addition, higher tissue levels of omega 3 are associated with significantly reduced all-cause, cardiovascular, and cancer mortality.

Omega-3 fatty acids are the chemical precursors of SPMs, specialized pro-resolving lipid mediators which help resolve inflammation. We know that cardiovascular events are driven by chronic inflammation in the walls of arteries, often mediated by insulin resistance. Chronic inflammation contributes to atherosclerosis (production of plaque in the artery wall) as well as cardiovascular events that result when unstable plaque ruptures. Studies suggest that n-3 fatty acids may have antiarrhythmic properties with membrane-stabilizing effects in addition to antithrombotic and anti-inflammatory properties on the endothelial level. Basic science, observational studies and clinical trials have demonstrated that higher tissue levels of omega 3 fatty acids are associated with longer health span and lifespan. This understanding must be balanced with a probable increased risk of AF in certain clinical situations associated with high dose omega-3 supplements as described above (people with known CAD, high risk for CAD, or following and MI). Note that current AHA and ACC dietary guidelines include at least 2 servings of fatty fish per week, one serving provides approximately 1800 mg of omega-3.

Getting omega-3 fatty acids from cold water fatty fish would be ideal. Unfortunately, many individuals do not like salmon, sardines, mackerel or herring and simply will not consume enough of this fish to achieve protective tissue levels. Other species of fish and seafood provide much less amounts of omega 3. Another consideration is that individuals process omega 3 fats differently so different amounts of omega 3 will be necessary to reach the same protective levels in tissue. You can obtain a red blood cell omega-3 index using a home kit and a finger prick without a prescription (https://omegaquant.com/). The sample is mailed in to the lab and results reported directly to you. I have no financial relationship with these folks.

Bill Harris, PhD, is widely published in the area of omega-3 science. He developed the first clinically useful tissue assay which measures the % of omega 3 fat in red blood cell membranes, the “omega-3 index” which is the gold standard for omega 3 research and clinical testing. Although serum levels correlate with the red blood cell index, the later reveals dietary consequences of a 2-3 month period while serum levels reflect just a few days of most recent dietary habits. The red blood cell omega 3 index is analogous to the hemoglobin A1c which reveals average blood sugars over a 2–3-month period. Bill Harris suggests that 1800 mg per day of omega 3 fat consumption (food plus supplements) will achieve an index of >= 8% in most individuals.

Here are some references.

Harris WS, Tintle NL et.al., Fatty Acids and Outcomes Research Consortium (FORCE). Blood n-3 fatty acid levels and total and cause-specific mortality from 17 prospective studies. Nat Communications. 2021 Apr 22;12(1):2329. doi: 10.1038/s41467-021-22370-2. PMID: 33888689; PMCID: PMC8062567. https://pubmed.ncbi.nlm.nih.gov/33888689/

“Here we report the results of a de novo pooled analysis conducted with data from 17 prospective cohort studies examining the associations between blood omega-3 fatty acid levels and risk for all-cause mortality. Over a median of 16 years of follow-up, 15,720 deaths occurred among 42,466 individuals. We found that, after multivariable adjustment for relevant risk factors, risk for death from all causes was significantly lower (by 15-18%, at least p < 0.003) in the highest vs the lowest quintile for circulating long chain (20-22 carbon) omega-3 fatty acids (eicosapentaenoic, docosapentaenoic, and docosahexaenoic acids). Similar relationships were seen for death from cardiovascular disease, cancer and other causes”

Blood Levels of Long-Chain n–3 Fatty Acids and the Risk of Sudden Death Authors: Christine M. Albert, M.D., M.P.H., Hannia Campos, Ph.D., Meir J. Stampfer, M.D., Dr.P.H., Paul M. Ridker, M.D., M.P.H., JoAnn E. Manson, M.D., Dr.P.H., Walter C. Willett, M.D., Dr.P.H., and Jing Ma, M.D., Ph.D.

Published April 11, 2002 N Engl J Med 2002;346:1113-1118DOI:10.1056/NEJMoa012918 VOL. 346 NO. 15 https://www.nejm.org/doi/full/10.1056/NEJMoa012918

We conducted a prospective, nested case–control analysis among apparently healthy men who were followed for up to 17 years in the Physicians’ Health Study. The fatty-acid composition of previously collected blood was analyzed by gas–liquid chromatography for 94 men in whom sudden death occurred as the first manifestation of cardiovascular disease and for 184 controls matched with them for age and smoking status.

RESULTS

Base-line blood levels of long-chain n–3 fatty acids were inversely related to the risk of sudden death both before adjustment for potential confounders (P for trend = 0.004) and after such adjustment (P for trend = 0.007). As compared with men whose blood levels of long-chain n–3 fatty acids were in the lowest quartile, the relative risk of sudden death was significantly lower among men with levels in the third quartile (adjusted relative risk, 0.28; 95 percent confidence interval, 0.09 to 0.87) and the fourth quartile (adjusted relative risk, 0.19; 95 percent confidence interval, 0.05 to 0.71).

CONCLUSIONS

The n–3 fatty acids found in fish are strongly associated with a reduced risk of sudden death among men without evidence of prior cardiovascular disease.

Heydari B, Abdullah S, Pottala JV, Shah R, Abbasi S, Mandry D, Francis SA, Lumish H, Ghoshhajra BB, Hoffmann U, Appelbaum E, Feng JH, Blankstein R, Steigner M, McConnell JP, Harris W, Antman EM, Jerosch-Herold M, Kwong RY. Effect of Omega-3 Acid Ethyl Esters on Left Ventricular Remodeling After Acute Myocardial Infarction: The OMEGA-REMODEL Randomized Clinical Trial. Circulation. 2016 Aug 2;134(5):378-91. doi: 10.1161/CIRCULATIONAHA.115.019949. PMID: 27482002; PMCID: PMC4973577. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.115.019949

Conclusions: Treatment of patients with acute myocardial infarction with high-dose omega-3 fatty acids was associated with reduction of adverse left ventricular remodeling, noninfarct myocardial fibrosis, and serum biomarkers of systemic inflammation beyond current guideline-based standard of care.

Effect of Different Antilipidemic Agents and Diets on Mortality A Systematic Review

Studer M, Briel M, Leimenstoll B, Glass TR, Bucher HC. Effect of Different Antilipidemic Agents and Diets on Mortality: A Systematic Review. Arch Intern Med. 2005;165(7):725–730. doi:10.1001/archinte.165.7.725

Compared with control groups, risk ratios for cardiac mortality indicated benefit from statins (0.78; 95% CI, 0.72-0.84), resins (0.70; 95% CI, 0.50-0.99) and n-3 fatty acids (0.68; 95% CI, 0.52-0.90).

Feuchtner G, Langer C, Barbieri F, Beyer C, Dichtl W, Friedrich G, Schgoer W, Widmann G, Plank F. The effect of omega-3 fatty acids on coronary atherosclerosis quantified by coronary computed tomography angiography. Clin Nutr. 2021 Mar;40(3):1123-1129. doi: 10.1016/j.clnu.2020.07.016. Epub 2020 Jul 22. PMID: 32778459. https://pubmed.ncbi.nlm.nih.gov/32778459/

Conclusions: Omega-3-PUFA supplementation is associated with less coronary atherosclerotic “high-risk” plaque (lipid-rich) and lower total non-calcified plaque burden independent on cardiovascular risk factors. Our study supports direct anti-atherogenic effects of Omega-3-PUFA.

Alfaddagh A, Elajami TK, Saleh M, Mohebali D, Bistrian BR, Welty FK. An omega-3 fatty acid plasma index ≥4% prevents progression of coronary artery plaque in patients with coronary artery disease on statin treatment. Atherosclerosis. 2019 Jun;285:153-162. doi: 10.1016/j.atherosclerosis.2019.04.213. Epub 2019 Apr 13. PMID: 31055222; PMCID: PMC7963401.An omega-3 fatty acid plasma index ≥4% prevents progression of coronary artery plaque in patients with coronary artery disease on statin treatment – PMC (nih.gov)

Conclusions: EPA and DHA added to statins prevented coronary plaque progression in nondiabetic subjects with mean LDL-C <80 mg/dL, when an omega-3 index ≥4% was achieved. Low omega-3 index <3.43% identified nondiabetic subjects at risk of coronary plaque progression despite statin therapy

Association of Plasma Phospholipid Long-Chain Omega-3 FattyAcids with Incident Atrial Fibrillation in Older Adults: The Cardiovascular Health Study, Circulation Volume 125, Number 9 https://doi.org/10.1161/CIRCULATIONAHA.111.062653

Among 3326 US men and women ≥65 years of age and free of AF or heart failure at baseline, plasma phospholipid levels of eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid were measured at baseline by use of standardized methods. Incident AF (789 cases) was identified prospectively from hospital discharge records and study visit ECGs during 31 169 person-years of follow-up (1992-2006).

Conclusions: In older adults, higher circulating total long-chain n-3 PUFA and docosahexaenoic acid levels were associated with lower risk of incident AF (atrial fibrillation). These results highlight the need to evaluate whether increased dietary intake of these fatty acids could be effective for the primary prevention of AF.

Omega-3 Fatty Acid Therapy: The Tide Turns for a Fish Story https://www.mayoclinicproceedings.org/article/S0025-6196(16)30764-9/fulltext

An omega-3 index of less than 4% is associated with increased CHD risk, particularly for sudden cardiac death. In contrast, an omega-3 index of more than 8% is associated with low CHD risk, whereas the range between 4% and 8% is considered intermediate risk

Risk of sudden death

Alfaddagh A, Elajami TK, Ashfaque H, Saleh M, Bistrian BR, Welty FK. Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients with Coronary Artery Disease: A Randomized Clinical Trial. J Am Heart Assoc. 2017; 6: e006981. 10.1161/JAHA.117.006981. https://pubmed.ncbi.nlm.nih.gov/29246960/

“High-dose eicosapentaenoic acid and docosahexaenoic acid provided additional benefit to statins in preventing progression of fibrous coronary plaque in subjects adherent to therapy with well-controlled low-density lipoprotein cholesterol levels.”

Huh JH, Jo SH. Omega-3 fatty acids and atrial fibrillation. Korean J Intern Med. 2023 May;38(3):282-289. doi: 10.3904/kjim.2022.266. Epub 2022 Dec 14. PMID: 36514212; PMCID: PMC10175873 https://pubmed.ncbi.nlm.nih.gov/36514212/

Effects of omega-3 fatty acid supplementation on the risk of atrial fibrillation. HR, hazard ratio; CI, confidence interval; VITAL, Vitamin D and Omega-3 Trial; ASCEND, A Study of Cardiovascular Events in Diabetes; STRENGTH, Statin Residual Risk with Epanova in High Cardiovascular Risk Patients with Hypertriglyceridemia; RP, Risk and Prevention Study; REDUCE-IT, Reduction of Cardiovascular Events With Icosapent Ethyl-Intervention Trial; GISSI-HF, Gruppo Italiano per lo Studio della Sopravvivenza nell’Insufficienza Cardiaca-Heart Failure; OMEMI, Omega-3 Fatty Acids in Elderly With Myocardial Infarction. Effects of omega-3 fatty acid supplementation on the risk of atrial fibrillation. HR, hazard ratio; CI, confidence interval; VITAL, Vitamin D and Omega-3 Trial; ASCEND, A Study of Cardiovascular Events in Diabetes; STRENGTH, Statin Residual Risk with Epanova in High Cardiovascular Risk Patients with Hypertriglyceridemia; RP, Risk and Prevention Study; REDUCE-IT, Reduction of Cardiovascular Events With Icosapent Ethyl-Intervention Trial; GISSI-HF, Gruppo Italiano per lo Studio della Sopravvivenza nell’Insufficienza Cardiaca-Heart Failure; OMEMI, Omega-3 Fatty Acids in Elderly With Myocardial Infarction. Effects of omega-3 fatty acid supplementation on the risk of atrial fibrillation. HR, hazard ratio; CI, confidence interval; VITAL, Vitamin D and Omega-3 Trial; ASCEND, A Study of Cardiovascular Events in Diabetes; STRENGTH, Statin Residual Risk with Epanova in High Cardiovascular Risk Patients with Hypertriglyceridemia; RP, Risk and Prevention Study; REDUCE-IT, Reduction of Cardiovascular Events With Icosapent Ethyl-Intervention Trial; GISSI-HF, Gruppo Italiano per lo Studio della Sopravvivenza nell’Insufficienza Cardiaca-Heart Failure; OMEMI, Omega-3 Fatty Acids in Elderly With Myocardial Infarction

THIS WEBSITE PROVIDES INFORMATION FOR EDUCATIONAL PURPOSES ONLY. CONSULT YOUR HEALTH CARE PROVIDER FOR MEDICAL ADVICE.

Doctor Bob

Study shows only 12% of US adults are metabolically healthy!

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What does this mean? The authors of this study looked at several important markers of health: waist circumference, fasting blood sugar, hemoglobin A1c, blood pressure, triglycerides, HDL, and whether someone was taking any medication related to these markers. They used data from the National Health and Nutrition Examination Survey 2009-2016. Only 12.3% of US adults qualified as healthy on all measures. So how did we get into this horrible situation?

Let’s step back and look at modifiable factors that play into these health measures.

Adequate restorative sleep
Stress
Nutrition
Exercise
Sunlight (Vitamin D)
Social connection
Environmental toxins
Rest

I have discussed the importance of sleep in several posts. Following this link you will find recommendations for good sleep habits that can enhance the quality and duration of your sleep.

If you have not watched Dan Pardi’s discussion of “HOW TO OPTIMIZE LIGHT FOR HEALTH” I recommend you watch this.

STRESS

Stress reduction is a huge topic. Managing stress involves so many areas it deserves a separate discussion. But here are some basics. Getting adequate sleep is the place to start. Activities like Meditation, Yoga, moderate exercise (walking outdoors in a green space) Tai Chi, music, practicing Mindfulness, and spending time with family and friends are all potential avenues to reduce the deletrious effects of stress in our lives.

NUTRITION

I have presented one approach to an anti-inflammatory diet and if you have not read through the details just follow the link. The low hanging fruit begins with elimination of processed foods, sweetened beverages, and pro-inflammatory “vegetable oils” (OILS made from corn, soy, cottonseed, safflower, sunflower, canola, margarine). EAT WHOLE FOODS.

TO LEARN ABOUT THE ILL-EFFECTS OF “VEGETABLE OILS” LISTEN TO NINA:

EXERCISE

My post about exercise as medicine can be found here.

The best way to exercise is to play as described by my friend Daryl Edwards in his TED talk.

Most Americans do not get enough, but some get too much. Moderation is important.

SUNLIGHT

Getting outdoor light exposure early in the day and avoiding the deleterious effects of artificial light in the evening (wear blue light blocking glasses in the evening) are two important ways to get the most benefit from light exposure, improve your sleep and enhance your Vitamin D level. Exercise outdoors in a green space provides more benefit than walking the treadmill indoors.

SOCIAL CONNECTION

Blue Zones are areas in the world that have the greatest numbers of individuals living to age 100. The climates and food varies among the various areas. They all have two things in common. First is a high degree of social connection, strong family ties, lifelong friends. Social connection within a supportive community is arguably one of the most important factors affecting health, longevity, and healthspan. Second, they eat REAL WHOLE FOOD.

blue zones longevity hotspots.jpg

ENVIORNMENTAL TOXINS

Part of eliminating environmental toxins includes consuming organic fruits and vegetables and eating meat, poultry and eggs from hormone-free, antibiotic-free, free- range/pastured sources. (ALL PART OF AN ANCESTRAL/PALEO DIET) If you are not familiar with the “dirty dozen” and the “clean 15” head on over to EWG.org where you will learn not only about what foods have the most/least residual pesticides, but also what personal care products and household cleaners are safe for you and your family.

WATER: Because humans have spent the last 4-5 decades polluting our air and water there is probably no water supply that is totally free of enviornmental toxins. To minimize your consumption of enviornmental toxins, filter your drinking water through a high quality system.

REST

Matthew Redlund MD has written a great book “THE POWER OF REST”. Here he discusses why sleep is not enough.

The fact that only 12% of American adults are metabolically healthy should be cause for great alarm. All chronic and degenerative diseases including dementia, heart disease, stroke, arthritis and cancer rise as metabolic health deteriorates.

Remember, this website offers educational information only. Consult your health care provider for medical advice.

Sleep well, exercise outdoors, laugh, love, engage in meaningful work, drink filtered water, eat clean, eat whole foods, get plenty of sunshine, spend time with those you love.

Doctor Bob

Ketogenic Diet, Keto-Medicine

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I have spent a few days watching lectures from various low-carb-healthy-fat meetings. There is an impressive amount of solid clinical data to support Very Low Carb (with healthy fat) diets to treat obesity, insulin resistance, diabetes, pre-diabetes, metabolic syndrome, and seizure disorders. Eric Westman MD, author, Associate Professor of Medicine, Past Chairman of the Obesity Medicine Association, and director of Duke University Lifestyle Medical Clinic gave an impassioned and authoritative talk on the success of LCHF in treating all of these disorders here.

Dr. Steven Phinney, Professor Emeritus UC Davis and presently Chief Medical Officer for VIRTA has given numerous talks on the beneficial effects of a ketogenic diet. He and Jeff Volek Ph.D. have done research for decades on the physiology of low carbohydrate diets. They elucidated the changes that occur in high level athletes as they adapt to burning fat as their major fuel source during and after a period of “fat adaptation”. It turns out that endurance athletes, after a period of 1 to 3 months of adaptation to a low carb-high fat diet (variable from person to person) perform at equal or higher levels as compared to their performance when previously on a high carbohydrate diet. In fact, because lean athletes have much greater energy stored in fat as compared to glycogen (carbohydrate) they can go for many hours longer than an athlete who is dependent on carbohydrate metabolism (not fat adapted). Glycogen is the starch source of energy that humans store in the liver (100 grams) and in muscle (400 grams). Compared to glycogen, fat stores in lean individuals, including buff athletes, can provide more than 10 times the amount of energy. Endurance athletes who are keto-adapted (fat burners) can ride a bike all day or run an ultra-marathon (100 miles) without taking in any energy source. (They must of course replace fluid and electrolytes). Whereas athletes who have followed a traditional high carb diet must start consuming calories after about 3 hours of moderate-high intensity exercise. Doctors Phinney and Volek have done clinical research on humans with obesity, pre-diabetes and diabetes and they have demonstrated superior results when compared to any other dietary approach.

You can learn about their work here:

And here:

So what is this all about? If carbohydrates are restricted to very low levels and instead we consume (healthy) fat as our major source of energy with moderate amounts of protein, then the human body starts to burn fat. This process results in the production of ketones (in the liver) which serve not only as a source of energy but also act as “signaling” molecules that turn on beneficial genes that fight inflammation and turn off genes that produce inflammation. When a well formulated ketogenic diet is followed under medical supervision, diabetics can often get off most or all of their diabetes medications within weeks to months as they lose weight. Improvements are seen quickly in blood pressure, fasting blood sugar, liver function tests, insulin sensitivity, inflammatory markers, subjective energy levels, mental clarity and mood. Triglycerides are reduced, HDL increases, and improvements are seen in the “atherogenic profile” with reductions in small dense LDL particles with a shift to large buoyant LDL particles. On a ketogenic diet humans spontaneously consume lower caloric intake because fat and protein are more satiating compared to carbohydrate. Circulating saturated fat in the blood DECREASES on a keto-genic diet. Refined carbohydrates and sugar (so prevalent in processed foods) produce increased circulating fat in the blood and increased fat storage throughout the body, often leading to fatty liver disease and the long list of chronic diseases caused by and associated with insulin resistance.

A ketogenic diet is also part of Dr. Dale Bredesen’s effective treatment program for early dementia (ReCoDe-Reversal of Cognitive Decline). I have discussed Dr. Bredesen’s approach before. Here is one of his discussions.

You can read Dr. Bredesen’s report of 100 patients who have reversed cognitive decline using a ketogenic diet as PART of the ReCoDe program here.

So what are the healthy fats in a low carb high fat diet?

They include fats found in whole foods such as nuts and avocados, pasture raised animals free of hormones and antibiotics, free range poultry and eggs, wild fish and seafood (avoiding large fish that have high mercury levels), extra virgin olive oil, avocado oil, butter from pastured grass-fed animals, and coconut oil. (yes butter is included despite that fact that strict paleo excludes dairy)

You should avoid all of the processed/refined oils that come from seeds, grains and legumes including soy oil, corn oil, cottonseed oil, canola oil, safflower oil, sunflower oil, sesame oil. You can learn why these (misnamed) “vegetable oils” are dangerous and how they were marketed to an unwitting public with the help and support of faulty science by listening to Nina Teicholz here:

There are many great lectures about the low-carb-high-fat ketogenic diet in addressing obesity, insulin resistance, pre-diabetes, metabolic syndrome, diabetes, seizures and more. Go to youtube and search “keto diet”, “low carb high fat”.

Before I sign off I will provide one more link:

Remember, this website offers educational information only. Consult your health care provider for medical advice.

Sleep well, exercise outdoors, laugh, love, engage in meaningful work, drink filtered water, eat clean, eat whole foods, get plenty of sunshine, spend time with those you love.

Doctor Bob

Western Diet (high sugar, refined carbs, unhealthy fats) alters genes and causes inflammation

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New study (in mice) shows fast food makes the immune system more aggressive in a detrimental way.

Major points:

The immune system reacts similarly to a high sugar, high (unhealthy) fat and high calorie diet as to a bacterial infection.
Unhealthy food seems to make the body’s defenses (innate immune system) more aggressive in the long term. Even long after switching to a healthy diet, inflammation towards innate immune stimulation is more pronounced.
These changes may be involved in the development of arteriosclerosis and diabetes.
These changes are due to alterations in gene transcription (up-regulation of genes associated with inflammation)
This up regulation of pro-inflammatory genes persists even after converting to a healthier diet.

Anti-inflammatory diet, are 9 servings of vegetables per day possible?

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I often recommend a specific diet to decrease inflammation, decrease pain, and improve healing of tissue. I have been asked by patients to post this nutritional plan on my website so here it is (see below). In addition to this post, I will place the diet on a separate page along with recipes for vegetable soup and bone broth.

The recipes (vegetable soup and bone broth) meet the anti-inflammatory diet guidelines and also follow the more restrictive “Autoimmune Protocol”. This nutritional approach provides an array of micro nutrients that fight inflammation, support tissue repair, decrease the risk of chronic disease, and help maintain a healthy gut flora (good bacteria in the intestines).

When I recommend 9 servings per day of vegetables patients often tell me it is impossible to achieve. But it is not impossible, nor is it impractical. Every Sunday afternoon I make a large pot of vegetable soup that will keep all week in the refrigerator. I bring generous servings to work every day for breakfast, brunch, and/or lunch and add some meat or seafood prepared the evening before (left-overs) on the side. The key to eating 9 servings per day is to have a variety of vegetables at every meal. The vegetable soup makes that goal not just achievable but convenient.

The anti-inflammatory diet described below provides ample fiber to feed your healthy gut bacteria and avoids the sugar and refined starches that can produce gut dysbiosis (unhealthy balance of bacteria in the intestines). Vegetables provide five times the amount of fiber per calorie compared to grains. You do not need to eat bread or cereal to get fiber.

So here is the anti-inflammatory diet. it is consistent with the Mediterranean diet as well as an Ancestral-Paleo diet.

Caution: if you have diabetes and are taking medications, this diet reduces carbohydrates and eliminates added sugar so adjustments in diabetes medications are necessary to avoid potentially dangerous low blood sugars. So consult your physician or primary care practitioner.

9 SERVINGS OF NON-STARCHY VEGETABLES PER DAY, 3 SERVINGS FROM EACH OF THREE CATEGORIES. Organic as much as possible. (Read about the Dirty Dozen here: Dirty Dozen | EWG’s 2017 Shopper’s Guide to Pesticides in Produce )

DARK GREEN LEAFY VEGETABLES, 3 SERVINGS PER DAY EQUALS 3 CUPS MEASURED COOKED OR 6 CUPS MEASURED RAW

Arugula, Beet Greens, Bok Choy, Chard all colors, Chicory, Cilantro
Dandelion Greens, Endive, Escarole, Kale-all kinds, Parsley, Radicchio
Radish leaves, Spinach, Turnip Greens, Watercress

Colored vegetables, 3 cups daily:

GREEN: Artichoke, Asparagus, Avocado (FRUIT), Cabbage (red and green) Celery, Cucumber with skin, Okra, Olives, Peppers, Zucchini with skin
RED: Beets, red cabbage, red peppers, cooked tomatoes (fruit)
YELLOW: Carrots, Pumpkin, Squash-summer and winter, Sweet potato,

SULFUR RICH VEGETABLES, 3 CUPS DAILY: Some leafy greens are also sulfur rich so there is overlap in these categories

Arugula, Asparagus, Bok Choy, Broccoli, Brussel sprouts, Cabbage, Cauliflower, Collard Greens, Garlic, Kale, Kohlrabi, Leeks, Mushrooms, Onions red-yellow-white, Radishes, Scallions, Shallots, Turnip Greens, Watercress.

Berries (any kind) ½ cup per day. This can be substituted for one serving of vegetables.

OMEGA-3 rich fish-seafood (at least 16 ounces per week)

Anchovies, clams, herring, mackerel, mussels, oysters, salmon, sardines, trout, calamari (squid), saltwater fish should be wild, shellfish farmed OK, farmed trout OK.

Meat ideally grass fed and grass finished, hormone and antibiotic free.

Poultry and eggs free range, any wild game meat or poultry.

Drink only filtered water, coffee, tea, bone broth (homemade is best) and kombucha.

No grains, cereal, bread, pasta, no food made from flour, no oats, wheat, barley, corn etc.

No legumes (beans), no peanuts

No dairy except Ghee for cooking (optional)

No processed food made with added sugar or hydrogenated oils (which contain trans-fats)

No “vegetable oils” (soy oil, corn oil, etc.)

Use only extra-virgin olive oil, coconut oil, avocado oil and ghee. Limit EVOO to low heat cooking or add after food is cooked. The other oils on this list have higher smoke points.

Do not use store-bought salad dressing which usually has added sugar and inflammatory vegetable oils. Make your own salad dressing with EVOO and vinegar or lemon juice.

For more information about the AIP (Autoimmune protocol) I suggest you visit these websites:

Autoimmune gut-repair diet – Autoimmune protocol | Dr. K. News

The Autoimmune Protocol – The Paleo Mom

The Autoimmune protocol is more restrictive than the anti-inflammatory diet and is beneficial for individuals with autoimmune disease.

Live clean, sleep well, exercise outside in the sunshine, love and laugh.

Dr. Bob

Don’t eat plastic foam in your food, another reason to avoid bread, bakery and flour foods

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I recently came across an article at EWG.org, Nearly 500 ways to make a yoga mat sandwich | EWG

“If you’ve planked on a yoga mat, slipped on flip-flops, extracted a cell phone from protective padding or lined an attic with foam insulation, chances are you’ve had a brush with an industrial chemical called azodicarbonamide , nicknamed ADA. In the plastics industry , ADA is the “chemical foaming agent ” of choice. It is mixed into polymer plastic gel to generate tiny gas bubbles, something like champagne for plastics. The results are materials that are strong, light, spongy and malleable. “

Turns out, ADA is in nearly five hundred foods including breads, tortillas, bagels, pizza, hamburger buns, various pastries, hot dog rolls, sandwich buns, Italian bread, bread sticks, dinner rolls, croutons, english muffins, focaccia, wheat bread. Not all food producers include ADA in their products but many do, including fast food chains.

“Over the years, health activists concerned about synthetic chemicals in food have attacked the widespread use of ADA, but it did not attract nationwide headlines until Hari of Food Babe circulated a petition demanding that Subway, among the nation’s biggest fast-food outlets, stop using the chemical in its loaves. Subway responded [http://www.subway.com/subwayroot/about_us/PR_Docs/QualityBread.pdf] that ADA was safe, but even so, it had quietly been seeking a substitute over the past year. The company pointed out that ADA is “found in the breads of most chains such as Starbuck’s, Wendy’s, McDonald’s, Arby’s, Burger King, and Dunkin Donuts.” Those other fast food giants joined Subway on the defensive.”

So head on over to the environmental working group website by clicking the link above and educate yourself. The reasons to avoid flour foods continue to mount, glyphosate (roundup), ADA, obesity, auto-immune disease, metabolic syndrome, diabetes, heart attack, stroke, endotoxemia…..

Live clean, sleep well, love and laugh.

Dr. Bob

Glyphosate update from Responsible Technology.org

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The Following comes directly from an e-mail newsletter discussing the increasingly alarming Glyphosate data.

Glyphosate poisoning is the emerging issue from decades of GMO Roundup Ready crops. Earlier this year, the UC San Diego released results from a long-term study that showed a 13x increase in the amount of glyphosate in urine tests of participants over a 20-year period. The State of California listed glyphosate as a known carcinogen effective July, 2017.

Glyphosate is in food, in the air, and in the water.

Glyphosate use in the agricultural sector rose 300-fold from 1974 to 2014. See Table. Glyphosate is also used liberally in landscaping, along roadways, railroad, and power company rights-of-way.

Review of facts.

The existing approval of glyphosate and Roundup is out of date. New research and the conclusions of an international team of reviewers have established ample reason to immediately discontinue use of Roundup and other herbicide formulations that contain glyphosate. Learn more about the documented health risks of glyphosate at RoundupRisks.com.

Be safe, eat only organic, non-GMO foods. Eat meat from animals that have not been exposed to GMOs, herbicides, pesticides, antibiotics or fed foods that are contaminated with these toxins.

Live clean, sleep well, laugh and love.

Dr. Bob

Practical Evolutionary Health

How food, exercise, sleep and stress affect your health, longevity, and happiness. How have we deviated from our evolutionary makeup?

Tag Archives: diet

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Effect of Different Antilipidemic Agents and Diets on Mortality A Systematic Review

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Study shows only 12% of US adults are metabolically healthy!

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Western Diet (high sugar, refined carbs, unhealthy fats) alters genes and causes inflammation

New study (in mice) shows fast food makes the immune system more aggressive in a detrimental way.

Anti-inflammatory diet, are 9 servings of vegetables per day possible?

Don’t eat plastic foam in your food, another reason to avoid bread, bakery and flour foods

Glyphosate update from Responsible Technology.org

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The scientific report guiding the US dietary guidelines: is it scientific?

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Blood Levels of Long-Chain n–3 Fatty Acids and the Risk of Sudden Death Authors: Christine M. Albert, M.D., M.P.H., Hannia Campos, Ph.D., Meir J. Stampfer, M.D., Dr.P.H., Paul M. Ridker, M.D., M.P.H., JoAnn E. Manson, M.D., Dr.P.H., Walter C. Willett, M.D., Dr.P.H., and Jing Ma, M.D., Ph.D.

Effect of Different Antilipidemic Agents and Diets on Mortality A Systematic Review

Omega-3 Fatty Acid Therapy: The Tide Turns for a Fish Story https://www.mayoclinicproceedings.org/article/S0025-6196(16)30764-9/fulltext

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New study (in mice) shows fast food makes the immune system more aggressive in a detrimental way.

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