Insulin is misunderstood by many, including patients and even physicians. Most physicians think of insulin as a hormone that pushes glucose into the cell by opening a channel. However, the truth is that insulin is primarily a fat-storage hormone and shifts metabolism from fat use as energy to fat as storage. In the absence of insulin, the default is to use fat storage and convert it to usable energy, known as lipolysis. In the presence of insulin, lipolysis stops and lipogenesis starts, converting circulating glucose to lipid (fat) storage.

The higher your insulin, the greater you push circulating glucose to glycogen and then to fat stores. The circulating glucose capacity is approximately 5g. The glycogen storage capacity is 500g. Comparatively, the storage capacity for fat is limitless (exceeding 100,000g). As your fat storage depots fill, they release inflammatory cytokines.

There are two examples of this, both dealing with different types of diabetes. Type 1 diabetics, our first example, have an autoimmune dysfunction that destroys beta cells, stopping insulin production. Type 1 Diabetics produce little to no insulin and are thin until we give them insulin. Once they get excessive insulin, these patients gain weight. The insulin becomes excessive because our dietary guidelines encourage six snacks and meals per day with approximately 40% carbohydrates. We are chasing the blood glucose with insulin because we are overfeeding carbohydrates.

The second example relates to type 2 diabetes. Well over 90% of type 2 diabetics are overweight because they consume too much carbohydrate and produce chronically elevated levels of insulin to compensate. They then become progressively more overweight, and the glycation of the cellular structures leads to rapid aging. This excessive insulin causes excessive fat storage and inflammation as the fat cells swell and leech inflammatory cytokines.

To lose weight and process insulin most effectively, we must recognize some simple truths about ketosis and carbohydrates. Nutritional ketosis is the default human state, and consuming mostly carbohydrates is the preparatory stage for fat storage now, so you can be in ketosis later.

When you spend more time out of ketosis than in ketosis, you will develop insulin resistance. However, more ketosis is not better — you need just enough that you are predominately using fat as fuel.

The debate should be what combination of healthy food and activity is necessary to achieve a predominant state of ketosis. Once we get to this debate, 2/3 of our current chronic health expenditures will magically evaporate.

Nutritional ketosis has been found to improve metabolic and inflammatory markers, including lipids, HbA1c, high-sensitivity CRP, fasting insulin, and glucose levels, as well as aid in weight management. We discuss these findings and elaborate on potential mechanisms of ketones for promoting weight loss, decreasing hunger, and increasing satiety. Humans have evolved with the capacity for metabolic flexibility and the ability to use ketones for fuel. When we are eating low numbers of carbohydrates, insulin levels remain low and ketogenesis takes place. These conditions promote the breakdown of excess fat stores, sparing of lean muscle, and improvement in insulin sensitivity.

Curr Nutr Rep. 2018 Sep;7(3):97-106. doi: 10.1007/s13668-018-0235-0.

Reverse Diabetes MD Presentation | Reverse Diabetes MD from Gurpreet Padda on Vimeo.

It’s time to take a more detailed look at the root causes of obesity, prediabetes, and type 2 diabetes because of the implication for future public health. Reversing the obesity, prediabetes, and type 2 diabetes epidemic is today’s most important public health challenge.  Nearly 70% of population is insulin resistant, prediabetic, or frankly diabetic.

Kraft, J.R.:” Glucose Insulin Tolerance. A routine Clinical Laboratory Tool Enhancing Diabetes Detection”. In O.B. Hunter. Jr. (ed): Radio assay: Clinical Concepts. Skokie, IL. Professional Education Dept. G.D. Searie& Co., 1974. Pp 91-106

Using data from the National Health and Nutrition Examination Survey 2009-2016, less than 12.2% of the US population is now considered metabolically healthy.

“Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009-2016,” was published online Nov. 28 in the journal Metabolic Syndrome and Related Disorders.

Almost all the patients who present to our clinics are overweight, and when we evaluate their biochemical markers, they have prediabetes and metabolic inflammation.  Pre-diabetes is known to be a condition that precedes type 2 diabetes (T2D).  The changes in immune cells concentration and function can cause an increased migration of these inflammatory cells to already inflammed tissue. There is also upregulation of cytokines. This immune activation begins during the pre-diabetic state.

According to studies published in a cardiovascular and heart disease prevention journal in Europe, “The increased risk of adverse cardiovascular outcomes associated with type 2 diabetes does not begin at the diagnostic cutoff for plasma glucose (or HbA1c) at which the condition is diagnosed. Rather, there appears to be a continuum of increased microvascular and macrovascular risk that extends to levels of glycemia well below these cutoffs.”

Hopper I, Billah B, Skiba M, Krum H. Prevention of diabetes and reduction in major cardiovascular events in studies of subjects with prediabetes: meta-analysis of randomized controlled clinical trials. Eur J Cardiovasc Prev Rehabil. 2011;18:813–823. [PubMed]

A 2015 global survey carried out by Credit Suisse revealed a substantial level of misinformation that exists among doctors and nutritionists:

• 92% believed that fat consumption could lead to cardiovascular issues
• 87% believed that fat consumption could lead to obesity
• 54% of doctors and 40% of nutritionists thought that eating cholesterol-rich foods raised blood cholesterol
• 83% of doctors believed butter was worse than margarine
• 66% of doctors believed vegetable oils are beneficial to health.

Fat; The New Health Paradigm – Credit Suisse 2015

The fact that prescription medications are now the third most common cause of death globally after heart disease and cancer should be alarming. The Academy of Medical Royal Colleges and the BMJ provide a blueprint to reduce the harms of “too much medicine” as part of the Choosing Wisely campaign, with recommendations to educate the public to ask their medical professionals whether there are “simpler or safer options” to taking a medication.

Malhotra A, Maughan D, Ansell J, Lehman R, Henderson A, Gray M et al. Choosing Wisely in the UK: The Academy of Medical Royal Colleges’ initiative to reduce the harms of too much medicine BMJ 2015; 350 :h2308.

The root cause of obesity, prediabetes, and type 2 diabetes are embedded in the food environment. Legislative efforts to encourage less consumption of processed foods and sugary drinks will help significantly reduce the burden of diet-related disease, which now contributes to more disease and death globally than physical inactivity, smoking and alcohol combined.

Newton JN, Briggs AD, Murray CJ, Dicker D, Foreman KJ, Wang H, et al. Changes in health in England, with analysis by English regions and areas of deprivation, 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2015. doi:10.1016/S0140-6736(15)00195-6.

Processed foods labelled as “low-fat” or “proven to lower cholesterol” should be avoided. The flawed science behind the 1977 Dietary Guidelines promoted a reduction in fat consumption, which permitted an increase in carbohydrate consumption.  The shift from natural food containing animal products and fats resulted in an increase in processed food consumption rich in carbohydrates, processed grains, and industrial seed oils. In the United States between 1961-2011, 90% of the increased calorie intake has come from carbohydrates and polyunsaturated vegetable oils.

Select Committee on Nutrition and Human Needs. Dietary goals for the United States. First ed. Washington: U.S. Govt. Print. Off., February 1977.

CreditSuisse.Fat: The New Health Paradigm: Research Institute, 2015: 76

 

The rise in obesity following these guidelines suggest that they may be a root cause of the problem. Nutrition science was originally founded on human correlational studies, which are frequently flawed. But that science has also been corrupted by commercial influences. The undue influence of the food industry on official guideline bodies and politicians has posed a significant threat to public health. “Nutritional epidemiology is a scandal. It should just go to the waste bin,” claims professor John Ioannidis, professor of medicine, health research and policy, and statistics  at Stanford University School of Medicine and School of Humanities and Sciences.

Max Planck also said, “Science progresses one funeral at a time.” it took nearly 50 years from the first published scientific evidence linking smoking and lung cancer until effective regulation was introduced to curb tobacco consumption. Big tobacco companies adopted a strategy of denial, planting doubt, obfuscating, and even buying the loyalty of scientists. The recent similarities with big food and big pharma are uncanny.

Brownell KD, Warner KE. The perils of ignoring history: big tobacco played dirty and millions died. How similar is big food? Milbank Q 2009;87: 259–94.

The food industry has a fiduciary responsibility to produce profit for their shareholders. Unfortunately, the food industries’ downstream cost to public health is bankrupting most westernized societies. Unfortunately, academics, institutions and journals whose primary responsibility is to patients and scientific integrity have at times colluded with industry for financial gain.  It is incredulous to suggest that consuming 22 teaspoons of sugar daily falls within recommended guidelines. This is despite the known science that for optimum health there is no dietary or biological requirement for sugar to be consumed in the human diet.

Malhotra, A. (2013) The dietary advice on added sugar needs emergency surgery. BMJ, 346, f3199.

 

Evidence from multiple randomized controlled trials reveals that a higher-fat, lower-carbohydrate diet is superior to a low-fat diet for weight loss and cardiovascular disease risk reduction. A meta-analysis of 53 randomized controlled trials involving 68,128 participants conducted by the Harvard School of Public Health concluded that “when compared with dietary interventions of similar intensity, evidence from randomized controlled trials does not support low-fat diets over other dietary interventions for long-term weight loss. In weight loss trials, higher-fat weight loss interventions led to significantly greater weight loss than low-fat interventions.”

Sackner-Bernstein J, Kanter D, Kaul S. Dietary Intervention for Overweight and Obese Adults: Comparison of Low-Carbohydrate and Low-Fat Diets. A Meta-Analysis. PLoS One 2015;10(10):e0139817 DOI: 10.1371/journal.pone.0139817[published Online First: Epub Date]|.

Bazzano LA, Hu T, Reynolds K, et al. Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial Effects of Low-Carbohydrate and Low-Fat Diets. Ann. Intern. Med. 2014;161(5):309-18 DOI: 10.7326/M14-0180[published Online First: Epub Date]|.

Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomized controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2(1) DOI: 10.1136/openhrt-2014-000196[published Online First: Epub Date]|.

 

The Women’s Health Initiative, one of the largest randomized controlled diet trials ever performed, used 48,835 post-menopausal women, with a mean follow-up period of 8.1 years, randomized to either a standard western diet or a low-fat, calorie-reduced diet with increased exercise.   The authors had postulated that a low-fat, calorie-reduced diet with increased exercise would reduce cardiovascular disease. The intervention achieved an 8.2% energy decrease in total fat intake and a 2.9% energy decrease in the saturated fat intake but did not reduce risk of CHD or stroke. The reduction in dietary fat and total daily calories (361 calories/day reduction) failed to produce any significant weight loss over the duration of the study, thus rejecting the hypothesis that the low-fat diet is either beneficial for cardiovascular disease or weight loss.

Howard BV, Van Horn L, Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: The Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006;295(6):655-66 doi: 10.1001/jama.295.6.655[published Online First: Epub Date]|.

By contrast, consumption of fat induces satiation and when compared to the other macronutrients such as protein and carbohydrates,  fat has the least impact on blood glucose and insulin production. Excessive insulin production and subsequent insulin resistance is the precursor to type 2 diabetes.  A meta-analysis of the evidence available prior to the 1977 US change in dietary guidelines did not support the dietary fat restrictions. Despite the lack of scientific consensus, these guidelines advised to limit total fat to 30% of calorie intake and saturated fat to 10% of calorie intake, creating the low-fat craze and a national experiment on diet-induced metabolic dysfunction.

Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomized controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart 2015;2(1) doi: 10.1136/openhrt-2014-000196[published Online First: Epub Date]|.

 

Thirty years later, in 2014, a meta-analysis of 76 studies with over 600,000 participants from 18 countries concluded that “Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Chowdhury R, Warnakula S, Kunutsor S, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann. Intern. Med. 2014;160(6):398-406 doi: 10.7326/M13-1788[published Online First: Epub Date]|.

 

A study published in the BMJ (British Medical Journal) noted that “Saturated fat intake was not associated with all- cause mortality, CVD mortality, total CHD, ischemic stroke, or type 2 diabetes.”

de Souza RJ, Mente A, Maroleanu A, et al. Intake of saturated and trans unsaturated fatty acids and risk of all-cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. BMJ 2015;351 doi: 10.1136/bmj.h3978[published Online First: Epub Date]|.

 

Further, The American Journal of Clinical Nutrition found that “diets with cheese and meat as primary sources of saturated fatty acids cause higher HDL cholesterol and apo A-1 and, therefore, appear to be less atherogenic than is a low-fat, high- carbohydrate diet.”

Thorning TK, Raziani F, Bendsen NT, Astrup A, Tholstrup T, Raben A. Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial. The American journal of clinical nutrition 2015 doi: 10.3945/ajcn.115.109116[published Online First: Epub Date]|.

 

Full-fat dairy may protect against obesity.  A 2014 study concluded: “Participants in the highest tertile of whole-fat dairy intakes (milk, cheese, yogurt) had significantly lower odds for being obese. “

Crichton GE, Alkerwi Aa. Whole-fat dairy food intake is inversely associated with obesity prevalence: findings from the Observation of Cardiovascular Risk Factors in Luxembourg study. Nutrition Research 2014;34(11):936-43 doi: 10.1016/j.nutres.2014.07.014[published Online First: Epub Date]|.

 

Cohort studies confirm that plasma saturated fatty acids from dairy sources such as cheese and yogurt are inversely related to the incidence of type 2 diabetes. By contrast, the plasma saturated fat palmitic acid, linked to the consumption of starch, sugar and alcohol, is strongly associated with the development of type 2 diabetes.

Mozaffarian D. Saturated fatty acids and type 2 diabetes: more evidence to re-invent dietary guidelines. Lancet Diabetes Endocrinol 2014;2:770–2

Natural, non-processed, non-refined food (meat, fish, eggs, nuts, seeds, olive, avocados) contains high levels of saturated fat. These natural foods are a portion of the ancestral human diet.  People have eaten as much as they want to of these foods without adverse health consequences since paleolithic times, until 1977 when the Dietary guidelines demonized saturated fat of omnipresent natural fat, driving people away from highly nourishing, wholesome and health-promoting foods.

Reducing dietary saturated fats does not reduce cardiovascular events and death. Improvements in cardiovascular outcomes are independent of direct cholesterol lowering. Dietary trials that provide abundant natural fats such as α-linoleic acid, polyphenols and Ω-3 fatty acids found in nuts, olive oil, oily fish and vegetables exert a positive health effect, likely by reducing inflammation, atherosclerosis and thrombosis.

Chakrabarti S, Freedman JE. Review: nutriceuticals as antithrombotic agents. Cardiovasc Ther 2010;28:227–35.

Interestingly, replacing saturated fat with Ω-6 containing vegetable oils (highly processed and refined industrial seed oil) does lower LDL cholesterol but does not actually improve cardiovascular mortality, and may actually increase mortality.

Veerman J Lennert. Dietary fats: a new look at old data challenges established wisdom BMJ 2016; 353 :i1512

Total and LDL cholesterol are a poor marker of cardiovascular health.  Cholesterol profile of elevated triglycerides and low HDL is a more predictive marker of cardiac risk and a reliable marker of insulin resistance. In fact, the QRISK calculator, used to estimate the 10-year risk of CVD, does NOT use LDL cholesterol, but uses total cholesterol/HDL ratio instead.

Preventing insulin resistance in young men would prevent 42% of myocardial infarctions, a larger reduction than correcting hypertension (36%), low high-density lipoprotein cholesterol (31%), body mass index (21%) or low-density lipoprotein cholesterol (16%).

Eddy D, Schlessinger L, Kahn R, Peskin B, Schiebinger R. Relationship of insulin resistance and related metabolic variables to coronary artery disease: a mathematical analysis. Diabetes Care. 2009;32(2):361–6.

 

Refined Carbohydrates:

Prediabetes and Type 2 diabetes are diseases of insulin resistance with initial excessive insulin production, which display the symptom of elevated blood glucose levels as the disease progresses. Treating the root cause of the disease, instead of the symptom, is the key. Eliminate all refined carbohydrates to reverse obesity, prediabetes, and type 2 diabetes.

Refined carbohydrates are known to increase blood glucose levels, increase requirements for medications and result in weight gain. It is disturbing that dietary guidelines prioritize the consumption of starchy carbohydrates for type 2 diabetics, to nearly 55% of their daily macronutrient consumption. Such diets will potentially lead to progressive worsening of disease with all its attendant complications, such as blindness, kidney failure, nerve damage, peripheral vascular disease, heart disease and stroke.

Added sugar has no nutritional value whatsoever. There are no biochemical reactions in the human body that require dietary fructose. No single study exists that demonstrates benefit associated with its consumption.

Credit Suisse – Sugar Consumption at a crossroads

Dietary carbohydrate restriction is the “single most effective intervention for reducing all of the features of the metabolic syndrome” according to Credit Suisse, and should be the first approach in diabetes management. A ketogenic diet (one that comprises less than 10 percent of calorie intake from carbohydrates) results in the greatest falls in HbA1C and reduction in the use of medications. These benefits accrue independently of weight loss.

Feinman RD, Pogozelski WK, Astrup A, et al. Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition 2015;31:1–13.

Sugar+veg oil+grain=obesity®PreDM®T2D

Dietary sugar is strongly associated with increased risk of type 2 diabetes, hypertension, and cardiovascular disease, independent of its calories or its effects on body weight.

Lustig RH: Sickeningly sweet: does sugar cause type 2 diabetes? YES. Can J Diab (in press).

Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome. Lustig RH, Mulligan K, Noworolski SM, Tai VW, Wen MJ, Erkin-Cakmak A, Gugliucci A, Schwarz JM. Obesity (Silver Spring). 2016 Feb;24(2):453-60. doi: 10.1002/oby.21371. Epub 2015 Oct 26.

Added sugar intake and cardiovascular diseases mortality among US adults. Yang Q, Zhang Z, Gregg EW, Flanders WD, Merritt R, Hu FB. JAMA Intern Med. 2014 Apr;174(4):516-24. doi: 10.1001/jamainternmed.2013.13563.

 

Vegetable Oil:

Despite at least 2-3 million years of human history, only since 1917 have industrial seed oils been a significant part of the human diet, with a major uptick in consumption in the late 1970s. Linoleic acid (the Ω-6 fat in these vegetable oils) is extremely susceptible to oxidation, making foods rancid, but also oxidizing in the body. Linoleic acid, in non-processed whole food (seeds, nuts, fish, and eggs), coexists with vitamins, minerals, and antioxidants, protecting this highly susceptible polyunsaturated fat.

Free Radic Biol Med. 2001 Dec 1;31(11):1388-95. The stomach as a bioreactor: dietary lipid peroxidation in the gastric fluid and the effects of plant derived antioxidants. Kanner J, Lapidot T.

Curr Atheroscler Rep. 2009 Nov;11(6):403-10. Impact of circulating esterified eicosanoids and other oxylipins on endothelial function. Shearer GC, Newman JW.

A meta-analysis including almost 10,000 patients confirmed that high intake of Ω-6 oils (from vegetable oils/margarines) increases the risk of death and heart disease compared to saturated fat plus trans fat. Human research data suggest that we should remove these vegetable oils from our food supply for optimal health.

29.BMJ. 2013 Feb 4;346:e8707. doi: 10.1136/bmj.e8707. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. Ramsden CE1, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR.

Older data was confounded by the inclusion of Ω- 3 polyunsaturated fatty acid intake. This misrepresented the health benefits of Ω–6. Other studies, such as the Anti-Coronary Club trial, confirm that Ω–6 PUFA increases death and coronary heart disease compared to animal fat.

Christakis G, Rinzler SH, Archer M t al. Effect of the anti-coronary club program on coronary heart disease. Risk-factor status. JAMA 1966;198:597–604

The LA Veterans trial found that cancer mortality increases with the consumption of Ω–6 rich vegetable oils.

Pearce ML, Dayton S. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet 1971;1:464-7.

Animal studies have also found that Ω–6 PUFA promotes the growth of experimentally induced cancers, whereas Ω–3 inhibits their growth. Ω–6 rich vegetable oil ( such as sunflower and corn oil), is linked to the increased risk of death, coronary heart disease, and cancer in humans as well as the growth of cancer in animal models.

Am J Epidemiol. 1998 Feb 15;147(4):342-52. Adipose tissue Ω–3 and Ω–6 fatty acid content and breast cancer in the EURAMIC study. European Community Multicenter Study on Antioxidants, Myocardial Infarction, and Breast Cancer. Simonsen N1, van’t Veer P, Strain JJ, Martin- Moreno JM, Huttunen JK, Navajas JF, Martin BC, Thamm M, Kardinaal AF, Kok FJ, Kohlmeier L.

Cancer Res. 1988 Dec 1;48(23):6642-7. Effect of different levels of Ω–3 and Ω–6 fatty acids on azoxymethane-induced colon carcinogenesis in F344 rats. Reddy BS, Sugie S.

 

Why eat less, move more fails:

A calorie is a calorie only if it is incinerated in a bomb calorimeter, and the heat given off measured. Biologically derived calories from different foods have entirely different metabolic effects on the human body.  Equal calorie portions of sugar, alcohol, meat or olive oil have widely differing effects on hormonal systems, including insulin and satiety signals such as cholecystokinin or peptide YY. It is irrelevant how many calories a portion of food on a plate contains. What matters is how our body responds to taking in and absorbing those calories, how they are metabolized, and the resulting level of satiety.

The current caloric reduction strategies promoted for weight loss are ineffective. Using the standard calorie reduction approach produces a probability of attaining a normal weight at 1 in 167, generating a greater than 99% failure rate.

Fildes A et al. Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. 2015;105: e54–e59

It is wrongly assumed that excessive caloric intake is the root cause of obesity. A calorie of food energy has different metabolic fates depending upon the hormonal stimulation. That same calorie may be used to generate body heat or stored as body fat. Obesity is a disease of failed energy partitioning, not one of total energy intake. The primary driver of this partitioning is the hormone insulin.  Insulin is specifically a fat storage growth hormone.

Focusing on calories in and calories out produces an inherent bias against high-fat food, which may be protective against obesity and related diseases.  The simplistic calorie focus results in a dietary guideline supportive of starch and sugar replacement of fat, which promotes insulin resistance.

It is our hope that shifting focus away from calories and emphasizing a dietary pattern that focuses on food quality rather than quantity will reduce obesity, related diseases, and cardiovascular risk.

Malhotra A, DiNicolantonio JJ, Capewell S. It is time to stop counting calories, and time instead to promote dietary changes that substantially and rapidly reduce cardiovascular morbidity and mortality. Open Heart 2015;2(1) doi: 10.1136/openhrt-2015-000273[published Online First: Epub Date]|.

Yo-yo dieting with rapid weight loss and regain from fad dieting is detrimental to health. Such ‘weight cycling’ contributes to hypertension, insulin resistance and dyslipidemia, resulting in increased mortality risk and worse cardiovascular outcomes.

Mann T, Tomiyama AJ, Westling E, et al. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol 2007;62:220–33.

LC + exercise ¹ health

In the Action for Health in Diabetes trial,  no cardiovascular benefits were found on a low-calorie diet combined with increased physical activity in type 2 diabetic patients.

(Despite the significant weight loss even up to the maximum follow-up of 13.5 years, no health benefits could be found. )

Wing RR, Bolin P, Brancati FL, et al. Look AHEAD Research Group. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. NEngl J Med 2013;369:145–54.

 

Exercise is not the solution:

It is widely accepted amongst the public and media that consuming more calories than we burn is the cause of the obesity epidemic, and therefore the solution is to just do more exercise.

Food and beverage companies have pushed this physical activity message to exonerate themselves. The very companies promoting processed and highly refined foods linked to the obesity epidemic have sponsored major sporting events.  This association of ultra-processed food and soft drinks with sport is troubling. Celebrity endorsements give the wrong message, particularly to children.

Regular physical activity does have beneficial health effects, but weight loss is not one of them. In fact, there has been little change in our levels of physical activity in the past three decades, while the levels of obesity have increased.

Luke A, Cooper RS. Physical activity does not influence obesity risk: time to clarify the public health message. Int J Epidemiol 2013;42:1831–6.

It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet . A Malhotra, T Noakes, S Phinney Br J Sports Med bjsports- 2015-094911Published Online First: 22 April 2015 doi:10.1136/bjsports-2015- 094911

 

The time spent not eating, is more important than the time spent eating. Snacking will make you fat.  It’s the chronic high insulin from the constant feeding.

There have been two major changes in our dietary habits since the 1970s, prior to the onset of the obesity epidemic. The change to a high-carbohydrate, low-fat diet has been well documented and has played an important role in causing obesity. However, the increase in meal frequency plays an equal if not larger role and has been largely ignored. In the 1970s, the average number of eating opportunities was three – breakfast, lunch and dinner. By 2005, that number had almost doubled. Now we eat breakfast, snack, lunch, snack, dinner and snack — and more often than not, each of these contains refined carbohydrates.

Cameron JD. 6 meals per day does not result in greater weight loss. Br J Nutr. 2010 Apr;103(8):1098-101

Popkin BM. Does hunger and satiety drive eating anymore? Am J Clin Nutr 2010;91:1342–7

 

Eating nearly continuously from the moment we arise to the moment we go to sleep becomes an opportunity to store food energy without a chance to burn it. Eating six times a day does not result in weight loss but tends to increase overall consumption of food.  Snacks are produced for convenience and shelf stability and are filled with refined carbohydrates and often supplemented with Ω–6 vegetable oil.  The hyper-processing of food contributes to a high glycemic index, and the grazing pattern of behavior results in a chronically elevated level of insulin, the fat storage hormone.

Reducing the frequency of our meals and eliminating snacking are simple ideas that were practiced widely before the obesity epidemic.

 

Additional references for RCT’s comparing low carb and low fat for weight loss

• Shai I, et al. Weight loss with a low-carbohydrate, mediterranean, or low-fat diet. N Engl J Med 2008;359(3);229–41.
• Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The A to Z Weight Loss Study: A Randomized Trial. JAMA. 2007;297:969–977.
• Brehm BJ, et al. A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. J Clin Endocrinol Metab 2003;88:1617–1623.
• Samaha FF, et al. A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. N Engl J Med 2003;348:2074–81.
• Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr. 2003 Mar;142(3):253–8.
• Aude YW, et al. The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial. Arch Intern Med. 2004;164:2141–2146.
• Volek JS, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition & Metabolism 2004, 1:13.
• Yancy WS Jr, et al. A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial. Ann Intern Med. 2004;140:769–777.
• Nichols-Richardsson SM, et al. Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet. J Am Diet Assoc. 2005;105:1433–1437.
• Krebs NF, et al. Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents. J Pediatr 2010;157:252-8.
• Summer SS, et al. Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet. Obesity (Silver Spring). 2011 Mar 31. [Epub ahead of print]
• Daly ME, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial. Diabet Med. 2006 Jan;23(1):15–20.
• Westman EC, et al. The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr. Metab (Lond.)2008 Dec 19;5:36.
• Halyburton AK, et al. Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive performance. Am J Clin Nutr 2007;86:580–7.
• Dyson PA, et al. A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects. Diabet Med. 2007 Dec;24(12): 1430-5.
• Keogh JB, et al. Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. Am J Clin Nutr 2008;87:567–76.
• Volek JS, et al. Carbohydrate Restriction has a More Favorable Impact on the Metabolic Syndrome than a Low Fat Diet. Lipids 2009;44:297–309.
• Partsalaki I, et al. Metabolic impact of a ketogenic diet compared to a hypocaloric diet in obese children and adolescents. J Pediatr Endocrinol Metab. 2012;25(7-8):697-704.

Time Restricted Feeding | Reverse Diabetes MD from Gurpreet Padda on Vimeo.

Time-restricted feeding.

Time-restricted feeding can help people move into a healthier lifestyle and reverse insulin resistance as well as maintain a healthy weight. Most people eat from the time they wake up until the time they go to bed; typically, they eat three main meals, multiple snacks, and often soda in between.  This pattern leads to chronic high insulin production, which fatigues the insulin receptors.  In addition, insulin is a fat storage hormone, and elevated insulin levels lead to fat accumulation in the liver, creating metabolic inflammation.

Your metabolism exists in two states – the “fed” (insulin high) state and the “fasted” (insulin low) state. Either we are storing food energy (increasing storage), or we are burning stored energy (decreasing storage or fat lysis).  If we start eating the minute we roll out of bed and do not stop until we go to sleep, we spend almost all our time in the fed state. Over time, we gain weight, because we have not allowed our body time to burn stored food energy.

Time-restricted feeding shortens the time window that a patient eats, shortening the “fed” state and lengthening the “fasted” state.  This reduces the total amount of insulin produced for the day.  Insulin is a fat-storage hormone, and a high level of insulin production leads to insulin resistance.  Time-restricted feeding is considered a type of fasting and has extraordinary benefits, including weight and body fat loss, lowered blood insulin and sugar levels, and a reversal of type 2 diabetes. Other possible benefits include improved mental clarity and concentration, a reduction in the risk of Alzheimer’s disease, activating of cellular cleansing by stimulating autophagy, and reduction of inflammation.

Time-restricted feeding is a type of fasting; it is not starvation.  Starvation is the involuntary absence of food for a long time, leading to severe suffering or even death. Starvation is not deliberate or controlled.  Fasting is the voluntary withholding of food. It’s done by someone who is not underweight and thus has enough stored body fat to live off. When done right, intermittent fasting should not cause suffering.  Food is easily available, but you choose not to eat it. You may begin a fast at any time of your choosing, and you may end a fast at will, too. You can start or stop a fast for any reason or no reason at all.  Any time that you are not eating, you are intermittently fasting. For example, you may fast between dinner and breakfast the next day, a period of approximately 12-14 hours. In that sense, intermittent fasting should be considered a part of everyday life.

The mere presence of insulin increases fat storage, and the absence of insulin permits lipolysis or fat usage as energy.

Lifestyle changes are key to managing obesity and Type 2 Diabetes, but by themselves don’t always control blood glucose levels. Bariatric surgery (gastric band or bypass) is effective but has significant risk. Drugs often manage the symptoms and may stave off complications, but don’t reverse the disease.

Time-restricted feeding has the potential to fill this gap in obesity and diabetes care by providing calorie restriction and the hormonal benefits of bariatric surgery without invasive surgery. Time-restricted feeding is defined as the controlled and voluntary abstinence from all calorie-containing food and drinks for a specified period of time.  During the fasting periods, patients are allowed to drink unlimited amounts of very-low-calorie fluids such as water, coffee, tea, and even bone broth. A general multivitamin supplement is encouraged to provide adequate micronutrients.

Metabolic flexibility:

Time-restricted feeding, or meal-timing strategy, reduces swings in hunger and alters fat and carbohydrate burning patterns, which may help with losing weight and improving insulin sensitivity.  It does not necessarily affect how many total calories patients burn but reduces the daily hunger swings and increases fat burning at night. It improves metabolic flexibility, which is the body’s ability to switch between burning carbs and burning fats.  Metabolic flexibility is the ease with which the body transitions between two different and opposing states, “fed” and “fasted,” without cravings or hunger pangs.

During feeding, insulin is elevated, which signals your body to store excess calories as fat. In the presence of insulin, the burning of fat is halted, while the body burns glucose instead.  In the fasted state, insulin is low (while glucagon and growth hormone increase), so the body mobilizes stored body fat from your fat cells and burns this fat for energy (instead of glucose).  You can only burn stored body fat while in the fasted state, and you can only store more body fat while in the fed state.

Most overweight patients live in a constant fed state, and rarely in a fasted state.  They continually burn glucose rather than fat at the cellular level. They have insulin resistance, caused by chronically high insulin levels, which promote fat storage and suppress fat mobilization.

When overweight “sugar burners” stops eating for even a few hours, they quickly run out of glucose from their last meal, instead of transitioning to the fasted state and burning stored body fat.  This causes acute brain signals of hunger and cravings for immediate sugar.  They spend most of the day trapped in a cycle of eating every few hours, spiking glucose, and then becoming hungry when blood sugar drops.  They may even develop low blood sugar and feel jittery; this is called reactive hypoglycemia.  This is a big clue that a patient lacks metabolic flexibility.

Fat-adapted energy use:

Your metabolic flexibility is determined by your mitochondria, the tiny energy factories inside the cells.  The mitochondria can burn both glucose (sugar) or fat for fuel, and over time they will develop a preference for one over the other; “sugar burners” have increased the pathways in the mitochondria that burn glucose and decreased pathways for burning fat.  As you become more metabolically flexible, the fat burning pathways will predominate, and you will become “fat adapted.”

Becoming fat adapted takes time and practice, and your body has to do a number of things to slowly up-regulate (or increase) your fat-burning pathways.  This includes improving insulin sensitivity to lower insulin and promote fat mobilization into free fatty acids and upregulating the fat-burning pathways at the cellular level (in the mitochondria).

Ways to improve fat adaptation include:

• Low-carbohydrate diets: A low-carb, high-fat (LCHF) diet improves the body’s ability to utilize fat for energy rather than glucose, as there is more fat and less glucose, even in the fed state.
• Exercise: High-intensity exercise depletes glucose and glycogen rapidly, forcing the body to switch to fat for fuel. Exercise also improves insulin sensitivity.
• Caloric restriction: Eating fewer calories also equals less glucose available for fuel, forcing the body to rely on stored body fat for fuel.
• Intermittent fasting forces the body to spend more time in the fasted state, giving the body more “practice” at burning fat.
• Supplementation: Ketone supplementation may be useful when first starting out. Ketones are breakdown products of fat, and when you first start out, ketones can reduce your hunger and provide energy for your mitochondria.

Patient education and engagement is the key to remission and curtailing the use of pharmacological interventions.  Morrison et al, also found that more frequent interactions with a provider led to markedly rapid reductions in serum glucose, HbA1C, and low-density lipoprotein cholesterol levels, followed up with the treating physician on average every 2 weeks.

How to do time-restricted feeding:

Our protocol can reverse obesity and Type 2 Diabetes (in individuals who still have the capacity to produce some insulin) by resensitizing the insulin receptor and restoring normal cyclical insulin production.  We restore the normal ebb and flow pattern of insulin, so the receptors are re-sensitized, and the constant high level of circulating insulin is reduced, reducing the fat storage action of insulin.

Time-restricted feeding is a type of intermittent fasting that limits your food intake to a certain number of hours each day.  An example of time-restricted eating is if you choose to eat all your food for the day in an 8-hour period, such as from 11 a.m. to 7 p.m., providing an 8-hour feeding window.  The remaining 16 hours are the fasting period, during which no calories are consumed.  This same schedule would be repeated every day.

Restricting feed times to a shorter window each day, starting at 8 hours/day and reducing by 1 hour per week down to 4-6 hours/day is highly effective in reversing diabetes and weight loss.  Medications must be clinically adjusted to prevent unintentionally low glucose levels or changes in blood pressure, which can be life-threatening.  To have success with this technique, cravings should be prevented.  Satiety is the key; you should not be hungry, or this will not be sustainable.  Food choice drives satiety.

Steps to success

Step 1

Before you start a time-restricted feeding schedule, you should talk to your doctor or health care provider. Get medical advice from a professional who is aligned with your health goals.

You may have medical conditions that need close monitoring. Likewise, you may be on medications that may need to be adjusted. It is important to have a strong understanding of your medical history and the medications you take prior to initiating a fasting program. Please talk to your doctor or healthcare provider.

Step 2

Stop all sugars, including all artificial sweeteners. Many sugars and processed carbs just aren’t satiating. Stop all sugar and artificial sugar sweetened beverages. Before you start your protocol, you should eliminate sugars and processed carbohydrates.

Stop all sources of vegetable oil and replace with healthy natural oil and real butter.  Replacing industrial seed oil with real oils is easy if you are not eating processed foods.  It even makes the food taste better.

Stop all processed foods.  Processed foods are engineered to make you eat again and again and again, every 2-3 hours.

Step 3

Focus on protein and healthy fats. Focus on getting meals that are rich in protein and healthy fats. Eat all types of meat like beef, fish, chicken, eggs, lamb, and seafood. Yogurt and cheeses are also nutritious and filling. Fill up on low-sugar vegetables like olives, peppers, cucumbers, and avocado, and eat as many green leafy vegetables as you please.  This approach will help you get better adapted to fat metabolism and may make fasting easier to adopt.

Step 4

Start slow.   This metainflammation didn’t happen in one day, and it won’t go away in a day. Consider a liberal 8-hour eating window on your first day to see how it feels. Eat as you please during your 8-hour time frame and see how your body and appetite feel during the remaining hours of the day.

Then, slowly narrow your eating window. As you feel more comfortable assessing your hunger and understanding the nature of hunger pangs, you can slowly decrease your daily feeding window. Consider decreasing by one hour a week, until you reach a 4-hour window.

Things to think about:

If you haven’t made adjustments to your diet beforehand to include more satiating foods filled with protein, healthy fat and fiber, you may notice hunger pangs. If you are experiencing hunger pangs, consider drinking some hot tea, coffee, water or seltzer. This will fill your stomach up and give you enough time to realize that maybe you really aren’t as hungry as you initially thought.  Some people use lemon in seltzer water.

This should be a fun experience, not a miserable experience.  If you are having a miserable experience, something has been overlooked.  Remember that time-restricted feeding is a  great way to limit snacking. Eating satiating real food during your eating window will restore and realign your hormone system.

Patients can reverse their diseases without the worry of side effects and financial burden of many pharmaceuticals, as well as the unknown long-term risks and uncertainty of surgery, all by means of time-restricted feeding.

Some practical tips:

• Don’t use time restricted feeding as an excuse to eat junk food when you are eating—continue to avoid processed foods.
• When you first start time-restricted feeding, you might have to supplement with a fast-mimicking substance like a ketone supplement.
• Check with your doctor before starting time-restricted feeding, especially if you are diabetic and on diabetes medications!
• You can generally take any vitamins or supplements you want while fasting as long as they don’t have calories, but you don’t need any supplements as you will be eating plenty of nutrient-dense foods every day. You may have to increase salt intake.
• You don’t have to worry about losing muscle from lack of protein during your fast, as long as you eat adequate protein at the meals before and after fasting. A LCHF (low-carb, high-fat) diet pairs nicely with intermittent fasting, as both improve fat adaptation a great deal.
• Exercising with time restricted feeding, either cardio or lifting weights (lifting weights is better), is acceptable. You will not lose muscle while fasting as long as you are exercising regularly.
• Drink plenty of water and non-caloric beverages while fasting; coffee and tea in the morning make fasting considerably more enjoyable in addition to health and fat-burning benefits and are highly recommended. You may have to increase salt intake.
• Skipping your morning meal gives your body more time to burn fat for energy. Hunger is lowest in the morning, so it may be easiest to skip it and break your fast later in the day.

Time-restricted feeding has many benefits but remains controversial. Diabetes medications will need to be adjusted. Discuss any changes in medication and relevant lifestyle changes with your doctor.  People who should not use time-restricted feeding include those who are underweight or have eating disorders, pregnant or breastfeeding women, and children under the age of 18.

Need more help? We have more to offer.

Additional references:

Suleiman Furmli, Rami Elmasry, Megan Ramos, Jason Fung. Therapeutic use of intermittent fasting for people with type 2 diabetes as an alternative to insulin. BMJ Case Reports, 2018; bcr-2017-221854 DOI: 10.1136/bcr-2017-221854

Morrison F , Shubina M , Turchin A . Encounter frequency and serum glucose level, blood pressure, and cholesterol level control in patients with diabetes mellitus. Arch Intern Med 2011;171:1542–50.doi:10.1001/archinternmed.2011.400

Duke S-AS , Colagiuri S , Colagiuri R . Cochrane Metabolic and Endocrine Disorders Group. Individual patient education for people with type 2 diabetes mellitus. Cochrane Database Syst Rev 2009;22.doi:10.1002/14651858.CD005268.pub2

Brethauer SA , Aminian A , Romero-Talamás H , et al . Can diabetes be surgically cured? Long-term metabolic effects of bariatric surgery in obese patients with type 2 diabetes mellitus. Ann Surg 2013;258:1.doi:10.1097/SLA.0b013e3182a5034b

Pucher PH , Lord AC , Sodergren MH , et al . Reversal to normal anatomy after failed gastric bypass: systematic review of indications, techniques, and outcomes. Surg Obes Relat Dis 2016;12:1351–6.doi:10.1016/j.soard.2016.01.030

Shoar S , Nguyen T , Ona MA , et al . Roux-en-Y gastric bypass reversal: a systematic review. Surg Obes Relat Dis 2016;12:1366–72.doi:10.1016/j.soard.2016.02.023

The University of Alabama at Birmingham. “Time-restricted feeding study shows promise in helping people shed body fat.” ScienceDaily. ScienceDaily, 6 January 2017. www.sciencedaily.com/releases/2017/01/170106113820.htm

Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? K. A. Varady. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1467-789X.2011.00873.x

Moro, T., Tinsley, G., Bianco, A., Marcolin, G., Pacelli, Q. F., Battaglia, G., … Paoli, A. (2016). Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males. Journal of translational medicine, 14(1), 290. doi:10.1186/s12967-016-1044-0. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064803/

Gabel, K., Hoddy, K. K., Haggerty, N., Song, J., Kroeger, C. M., Trepanowski, J. F., … Varady, K. A. (2018). Effects of 8-hour time restricted feeding on body weight and metabolic disease risk factors in obese adults: A pilot study. Nutrition and healthy aging, 4(4), 345–353. doi:10.3233/NHA-170036. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6004924/

Insulin, the most popular pharmaceutical treatment for type 2 diabetes, was once used only sparingly in diabetes treatment, but today makes lots of money for the manufacturers. Thanks to pharmaceutical marketing and a lack of time, many physicians prescribe insulin rather than nutritional counseling or lifestyle management.

Prior to the 1920s, the mainstay of Diabetes treatment was aimed at controlling glycosuria (glycosuria occurs when the blood glucose level exceeds about 160–180 mg/dL and is easily measured). These dietary recommendations consisted of “meats, poultry, game, fish, clear soups, gelatin, eggs, butter, olive oil, coffee, tea” and contained 5% carbohydrates, 20% protein, and 75% fat. This is analogous to the Low Carbohydrate Ketogenic Diet (LCKD) . These recommendations were dramatically different from current low-fat, high-carbohydrate recommendations for patients with diabetes.  Also note that the feeding frequency rarely included breakfast, and manufactured snacks were not yet invented, resulting in 2 low-level glucose spikes, as opposed to today’s 5-6 spikes.  Also, vegetable oils were not routinely available before the 1940s and 1950s. .

Exogenous insulin for the treatment of Diabetes was introduced in the 1920s, which began the switch to controlling diabetes through pharmaceutical management instead of lifestyle management, to the point that many type 2 Diabetic patients now consume excessive carbohydrates knowing they can chase it with insulin.  Unfortunately, these patients already have a high insulin level, and the extra insulin only makes the insulin resistance worse. Additionally, the fat storage action of insulin, makes the metainflammation worse as well as the patient’s obesity.  This is like a fat dog chasing its tail.  The glucose is the tail, the mouth is the insulin, and the fat dog is the metabolic derangement.

 

Several recent studies have re-examined the effect of carbohydrate restriction on type 2 Diabetes and revalidated the safety and efficacy of the Low Carbohydrate Ketogenic Diet (LCKD).  These studies confirmed that hemoglobin A1c improved to a greater degree over one year with a low-carbohydrate diet compared with a low-fat, calorie-restricted diet.  Specifically, the participants had greater improvement in glycohemoglobin while on the low-carbohydrate diet than when on a eucaloric low-fat diet.  Because LCKD can be very effective at lowering blood glucose, patients on diabetes medication who use this diet should be under close medical supervision or capable of adjusting their medication.

 

• Allen FM, Stillman E, Fitz R: Total dietary regulation in the treatment of diabetes: monograph No. 11. 1919, New York, The Rockefeller Institute for Medical Research Google Scholar
• Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams M, Gracely EJ, Samaha FF: The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med. 2004, 140: 778-785.View Article Google Scholar
• Samaha FF, Iqbal N, Seshadri P, Chicano K, Daily D, McGrory J, Williams T, Williams M, Gracely EJ, Stern L: A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med. 2003, 348: 2074-2081. 10.1056/NEJMoa022637.View Article Google Scholar  
• Gannon MC, Nuttall FQ: Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes. Diabetes. 2004, 53: 2375-2382.View Article Google Scholar
• Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP: Effect of a low-carbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med. 2005, 142: 403-411.View Article Google Scholar
• Nielsen JV, Jonsson E, Nilsson AK: Lasting improvement of hyperglycaemia and bodyweight: low-carbohydrate diet in type 2 diabetes. A brief report. Ups J Med Sci. 2005, 110: 179-183. Google Scholar
• Yancy WS, Vernon MC, Westman EC: Brief report: a pilot trial of a low-carbohydrate, ketogenic diet in patients with type II diabetes. Metabolic Syndrome and Related Disorders. 2003, 1: 239-244. 10.1089/154041903322716723.View Article Google Scholar

So, we know that patients with type 2 diabetes have the symptom of too much glucose, but their actual disease process is excessive Insulin, with the cells being insulin resistant; yet, we treat them with more insulin.  This begs the question, why and who benefits? (This is in no way to be construed as suggesting insulin is bad; insulin is a lifesaving drug.  It’s meant to suggest that patient therapy should be first geared to lifestyle changes, and insulin should be the rescue drug.)

Making lifestyle changes and counseling patients takes time and energy, which most healthcare providers lack.  As the one of the key decision makers, physicians remain a primary focus of pharmaceutical company sales success. The pharmaceutical industry employs numerous marketing and promotional efforts to influence prescribing patterns, starting early in medical school, even in the preclinical years of study. These marketing strategies continue throughout a physicians’ career.  Drug company marketing strategies include gifts and benefits ranging from low-cost gifts to expensive trips and grants, which leads to suboptimal prescribing practices and promotes more expensive medical treatment. One could postulate that most physicians are simply a marketing tool used by the pharmaceutical companies to get their products sold; they are an indirectly paid sales team.

Often, the pharmaceutical companies launder their education endeavors through patient advocacy groups that on the surface appear to be trusted authorities, such as The American Diabetes Association.

It is obvious that Big Pharma will not be likely to support studies that reduce the utilization of their products over non-compensable lifestyle changes.  Evidence-based academic research is also unlikely to be performed by academicians who are funded by these same interests.  The entire health delivery industry seems to be geared towards medicalization of treatment rather than lifestyle improvement, which would radically disrupt the status quo.  Big Pharma is so prevalent in the academic world of policy and thought leaders that it is no longer considered a “conflict of interest” to recommend a pharmaceutical that compensated that policy or thought leader. It is now simply considered a “duality of interest.”

Many people think that sugar is sugar, but there are different types and sugar comes in many forms. Compared with glucose, fructose plays a primary role in development of metainflammation, obesity, prediabetes, and type 2 diabetes

Fructose directly increases de novo lipogenesis, promotes dyslipidemia, decreases insulin sensitivity, increases visceral adiposity, and stimulates the reward center, similar to cocaine.

What is sugar?

Because glucose is the sugar that we most often talk about and measure in diabetics, most people assume that their regular table sugar is made of glucose. However, common table sugar is actually a disaccharide, made of two monosaccharides, fructose and glucose, bonded together in a 1:1 ratio.

High fructose corn syrup (HFCS) contains about 5% more fructose than glucose. HFCS is manufactured by hydrolyzing corn starch into glucose, which then is isomerized into fructose. Fructose is preferred by food and soft drink manufacturers because fructose exerts a significantly increased perception of sweetness and likely because its production is subsidized.  Glucose has a sweetness index of 74 compared to sucrose of 100 or fructose of 173.

According to the CDC, over 30 million Americans have diabetes, with 1 in every 4 not knowing their diagnosis. Fructose is more strongly linked to obesity and diabetes than glucose. There is no biochemical reaction in any eukaryotic organism that requires fructose.

Metabolism of glucose and fructose

Glucose can be utilized as an energy source by almost every cell in the body. Only the liver can metabolize fructose, and it will preferentially convert fructose into fat storage.  The body has the ability to handle a small amount of fructose at a time, without adverse health consequences. Fructose does come naturally from fruits, but the absorption is slow due to the large amount of fiber.  Unfortunately, removing the fiber by juicing or destroying the fiber, as done in a smoothie, dramatically increases the speed of absorption, overwhelming the liver and sending a fructose rush to the brain.

Glucose consumption normally causes insulin release from the pancreas. Insulin acts on surface cell receptors, which allow glucose absorption into the cell for energy use or converting it to fat inside the cell.  High levels of insulin, in the presence of high levels of glucose, cause a liver enzyme [phosphofructokinase PFK] to convert glucose to fructose, which is then quickly turned into fat storage and not used for energy production.  However, if you directly ingest fructose, it bypasses the enzyme gateway and insulin is not released, and it goes straight to fat storage.

The metabolism of fructose differs from that of glucose, with liver metabolism of fructose favoring de novo lipogenesis [fat production directly from fructose].  Additionally, fructose does not stimulate insulin secretion or leptin production. Insulin normally regulates the absorption of sugar into the cells, and leptin normally notifies brain receptors that you are full.  Because insulin and leptin act as key signals in the regulation of food intake and body weight, fructose consumption causes yet further hunger and additional weight gain.  The body is rapidly storing fat, and doesn’t know it’s full.

Insulin resistance from fructose and the beginning of metabolic inflammation

Fructose can also directly trigger insulin resistance. When mice are fed with excessive amounts of fructose, they produce carbohydrate responsive element-binding protein, or ChREBP, which blocks the liver from responding to the insulin.

Fructose is 20 times more likely to cause fatty liver (the key problem of insulin resistance) compared to glucose alone.  Fructose feeding studies, replacing glucose with a calorically equal amount of fructose, document  a 5x increase in de novo lipogenesis and an increased liver fat by 38% within eight days.

[The metabolism of ethanol (alcohol) is similar to that of fructose. Nearly 80% of the ingested ethanol is delivered to the liver, and metabolized to acetaldehyde, which also stimulates de novo lipogenesis.]

Fructose overfeeding can provoke insulin resistance. Healthy subjects overfed 1000 calories per day of fructose demonstrated a 25 percent worsening of their insulin sensitivity in seven days.

Fructose induces insulin resistance even at typical consumption doses, in less than eight weeks. Subjects were fed 25 percent of their daily calories as Kool-Aid sweetened with either glucose or fructose. The fructose group increased their insulin resistance, and could be clinically classified as pre-diabetic.  The glucose group did not.

Fructose engages in the Maillard reaction, or glycation seven times faster than glucose, and  a metabolite of fructose does it 250 times faster.  We commonly measure this as HgBA1C for glucose.  The measure for fructose is fructosamine.  This glycation effect makes the cell walls sticky, and the receptors not work.  This may explain why patients with high glycation levels require more pain medication, because their receptors simply don’t work.  It also is part of the explanation how insulin resistance occurs.

Fructose and addiction

Fructose stimulates the reward center of the brain while glucose does not.  Data suggests that the fructose molecule in sugar is what it makes it addictive.

 

• Glucose activates the cortex, the basal ganglia, and certain other parts, but not the limbic system.  Glucose results in a sensation of serotonin-induced happiness. By contrast, fructose stimulates the limbic system and is associated with increased dopamine release in the nucleus acumbens, similar to other addictive drugs (glucose does not stimulate the nucleus acumbens).  Fructose results in a sensation of dopamine-induced pleasure.

Agricultural subsidies

Governmental subsidies were initially a method to subsidize farmers during the Depression and the Dust Bowl in 1933.  We had a destitute population in the American southwest, dying of famine. Most of the the food and food manufacturers were in the Northeast.  By the time it took to transport food by rail to the Southwest, it would go rancid. They had to process it: remove the fiber from the  wheat, package it in 5 pound bags, ship it to the Southwest, and then bake it locally. The subsidy was designed to make it worthwhile for the American food industry to invest in a processing and distribution system for a famine-stricken population, which made sense through World War 2.

Unfortunately, President Nixon, concerned about re-election, knew that fluctuating food prices caused political unrest.  Nixon instituted a policy of maintaining low consumer prices for food by agricultural subsidy.  Until that point, our subsidies were actually designed to pay farmers to not grow certain crops and maintain inflated prices. This policy also allowed the soil to regain nutrient after crop harvest.  His agriculture secretary, Rusty Butz, changed farming operations so soil was no longer left fallow; there was no time to restore nutrient after a crop was harvested.  It also encouraged monocropping and megafarms.  Subsidies have created an agricultural farmer dependency on governmental support.  The massive overproduction of just a few grain items resulted in a huge surplus and difficulty in long-term storage.  Distributing this slowly rotting surplus was solved through the food stamp system, creating a consumer dependency on governmental support. Unfortunately, these processed staple items are carbohydrate-rich, but have had most of their fiber stripped and fat removed to prevent rancidity,  and lack much of the soil-derived micronutrients.

Governmental subsidies and import tariffs have resulted in corn being a much more economical sweetener than sugar–a trend that is not seen in other parts of the world.  The consumption of HFCS increased by more than 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents more than 40% of caloric sweeteners added to foods and beverages, a daily average of 132 calories per person. The effect of governmental subsidy is most evident when you compare the same soft drink in the United States to one in Mexico; for example, Coke contains corn syrup as the sweetener in the United States while it contains cane sugar in Mexico.

The per capita consumption of high fructose corn syrup — the primary sweetener in soft drinks and other sweetened beverages — has increased from 38.2 pounds in 1980 to 868 pounds in 1998 (Chou et al., 2004). In 1942, annual U.S. production of soft drinks was 90 8 oz. servings per person; in 2000, it was 600 servings (Jacobson, 2005).

Other names for sugars:

Processed foods will most likely have sugars added. Unfortunately, they can go by any number of names. While this is an extensive list, it is not complete. The more naturally you can eat your foods, the better success you will have with creating a permanent weight loss solution.

Agave Syrup

Amasake

Any name ending in “ose” or “ol” or “syrup”

Barbados Sugar

Barley Malt

Blackstrap Molasses

Black Sugar

Brown Sugar

Cane Juice or Cane Juice Crystals

Cane Sugar

Caramel or Caramel Coloring

Castor Sugar

Confectioner’s Sugar

Corn Sweetener

Corn Syrup – a manufactured syrup of corn

starch, containing varying proportions of glucose

maltose, and dextrose

Corn Syrup Solids

Crystallized Cane Juice

D-mannose

Date Sugar

Demerara

Demerara Sugar

Dehydrated Cane Juice or Dehydrated Cane

Juice Crystals

Dextran

Dextrin

Dextrine

 

Dextrose (glucose) – a simple sugar made of

only one molecule

Erythritol

Evaporated Cane Juice

Evaporated Cane Juice Sugar

Florida crystals (a trademarked name)

White or Brown Sugars

Fructose – a simple sugar refined from fruit

Fruit Juice Concentrate

Galactose or Galatactose

Glucose or Glucose Syrup

Golden Syrup

Grape Sugar

Grape Juice or Grape Sweetener

High Fructose Corn Syrup (HFCS)

Honey

Hydrolysed or Hydrolyzed Starch

Hydrogenated Glucose Syrup

Hydrogenated Starch Hydrolysates (HSH)

Invert Sugar

Isomalt

Levulose

Lactitol or Lactital

Lactose – a simple sugar from milk

Malt

Malt Extract

Malt Syrup

Maltodextrin

Maltose

Malitol

Maple Syrup

Molasses

Monosaccharide

Muscovado

Organic Dehydrated Cane Juice

Organic Brown Sugar

Panocha

Polysaccharide

Powdered Sugar

Raw Cane Crystals

Raw Honey

Raw Sugar

Understanding the risk factors that could lead to prediabetes and diabetes type 2… • Weight: Being overweight (have a body mass index—a BMI—of higher than 25), increases your risk for developing prediabetes. This is especially true if you carry a lot of extra weight in your abdomen. The extra fat cells can cause your body to become more insulin resistant.

• Being inactive: This often goes hand-in-hand with being overweight. If you aren’t physically active, you’re more likely to develop prediabetes.

• Having a close family member with type 2 diabetes: Prediabetes has a hereditary factor. If someone in your close family has (or had) it, you are more likely to develop it.

• Race/ethnicity: Certain ethnic groups are more likely to develop prediabetes, including African-Americans, Hispanic Americans, Native Americans, and Asian Americans.

• Age: The older you are, the more at risk you are for developing prediabetes. At age 45, your risk starts to rise, and after age 65, your risk increases exponentially.

• Gestational diabetes: If you developed diabetes while you were pregnant, that increases your risk for developing prediabetes later on.

• Other health problems: High blood pressure (hypertension) and high cholesterol (the “bad” LDL cholesterol) increase your risk of getting type 2 diabetes. • Polycystic ovary syndrome (PCOS) also raises the risk of prediabetes because it’s related to insulin resistance. •

Hypothyroidism (low thyroid function; not enough circulating thyroid hormone), and you have prediabetes, then your risk of developing T2D more than doubles in comparison to individuals with normal thyroid function.

• The Standard American Diet (SAD)