Cholesterol and Fats: Back to the Good Old Days!

A series of new studies and re-evaluation of old studies published over the past few months [1-6] have very clearly dispelled the myth that high levels of serum cholesterol or high intake of saturated fats are the causative factors for heart attacks or for increased mortality. It is about time for the world to accept that cholesterol or saturated fats are not our enemies, but sugars are.

Blaming and shaming of cholesterol and saturated fats started in the early 30s of the last century, got louder by the mid and late seventies, got stamped authoritatively by eighties. But the Diet- Heart hypothesis is being quietly shoved off almost half a century after its first proposal, and after tripling of metabolic diseases and after the deaths of millions due to coronary artery disease, stroke, hypertension and diabetes.

dietheartIn the early years of 19th century, sugars, fats and proteins were all blamed for atherosclerosis., diabetes and other modern diseases, with works of Warburg and Price pointing at sugars.[7-14] By 1955, Ancel Keys of Minnesota University fixed the blame on cholesterol and advised restriction of saturated fats to contain coronary artery disease.[15-17]

dietheart3But this was countered by Yudkin J and others, who attributed the rising incidence of modern diseases on rising consumption of sugars, rather than fats. According to Yudkin, the hypothesis of Ancel Keys and his collaborators that a high intake of fat, especially of saturated fat, was a potent cause of the disease was a false conclusion; and, in general, as populations become wealthier, their consumption of fat increases, and so does their consumption of sugar.[18-22] Campbell GD of The Diabetes Clinic, Durban also observed that the diabetes-prone have a diet consisting totally of refined carbohydrate; in almost every instance in tropical countries, as soon as per capita annual sugar intake passes 70 lb. per annum then diabetes becomes “common,“ and he proposed a “Rule of Twenty Years”, wherein he found strikingly constant period of exposure to ingestion of the Westernized diet before diabetes emerged and also “The Rule of the Ten Per Cent“, finding diabetes to be particularly common when the caloric intake of refined sugar exceeded 10 per cent of the total per capita caloric intake.[23]

But the debate turned nasty. Keys described Yudkin’s evidence as “flimsy indeed”. The British Sugar Bureau dismissed Yudkin’s claims as “emotional assertions“. Yudkin was “uninvited” to international conferences and his papers that attacked sugar were omitted from publications. And when Yudkin, in 1972, published his assertions as book titled ‘Pure, White and Deadly’, the World Sugar Research Organisation described his book as “science fiction“.[24,25]

dietheart2The Diet Heart Hypothesis became a juggernaut. The recommendations to reduce cholesterol in the diet, to reduce calories, to reduce fat, particularly saturated fats like whole milk, cheese, cream, butter, coconut oi, meat, to increase polyunsaturated fats like corn, cotton, soya oil etc., became mainstream and the American Heart Association, along with Keys, published and publicised these recommendations.[26] Even though the suggestions were emphatic, and later became worldwide dietary policy, the publication chose the words carefully: a reduction in blood cholesterol MAY lessen the development or extension of atherosclerosis and hence the risk of heart attacks or strokes, it said, and then went on to add a disclaimer that ‘it must be emphasised there is as yet no final proof that heart attacks of strokes will be prevented by such measures. There was no proof against cholesterol or fats, yet, it was suggested by AHA that reduction of cholesterol and fats may reduce heart attacks and strokes!

dietheart6Such wordplay did not weaken the Diet Heart Hypothesis, but strengthened it and Ancel Keys found a place on the cover of Time Magazine in 1963. In early 1977, the US Senate Select Committee on Nutrition and Human Needs recommended Dietary Goals for the American people and in February 1980, the Dietary Guidelines for Americans brochure was issued. It recommended to decrease dietary fat intake to no more than 30 percent of calories, with a reduction in intake of saturated fat, to decrease cholesterol intake to 300 mg per day, to increase carbohydrate intake to 55 to 60 percent of calories, to decrease sugar intake to 15 percent of calories and to decrease salt intake to 3 g per day.[27]

dietheart5There was no evidence against fats or cholesterol then, and it has not been obtained thereafter! A systematic review and meta-analysis of RCTs, published prior to 1983, which examined the relationship between dietary fat, serum cholesterol and the development of CHD, found no differences in all-cause mortality and non-significant differences in CHD mortality, resulting from the dietary interventions. The Government dietary fat recommendations were introduced in the absence of supporting evidence from RCTs and were untested in any trial, so much so, that a review had to be abandoned.[28,29]

On the other, evidence against sugar has kept mounting. In 1975, another ecological study using dietary supply data from 1963-1965 for 30 countries found sugar supply to have the highest correlation with ischemic heart disease mortality rates in 1968 or 1969 for both males and females.[29,30]

But, the low fat propaganda went on gaining momentum, and fat lowering became a $4 Trillion (Rs. 265L Crore) business, offering low fat food, fat reducing drugs, fat reducing exercises, fat reducing surgeries etc.!

Six decades after the low fat diet was first mooted and during the 3 decades from 1980s that low fat diet was drummed up, obesity and diabetes tripled and in the US, ½ of the adults developed one or more chronic diseases and ²⁄₃ of adults became obese or over weight [31-34] and many diseases like type 2 diabetes, hypertension, coronary artery disease etc., started striking the young, even children.[35-38]

dietheart7In these three decades, following the dietary guidelines of different Govts., the increased calories in our diets have come from sugars and other carbohydrates.  In the past 300 years too, sugar consumption has gone up by 50 times and diabetes has gone up from 3/lakh population in late 19th century to 8000/lakh by early 21st century.[39,40] Cross-sectional data on diabetes and nutritional components of food from 175 countries have shown that for  every 150 kcal/person/day increase in sugar availability (about one can of soda/day) the prevalence of diabetes increased by 1.1% (p <0.001) and that the duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner.[41] There are many other studies that have implicated sugars and carbohydrates in the pathogenesis of modern diseases.[42-49]

The report of the Joint WHO/FAO Expert Consultation on Diet, Nutrition and the Prevention of Chronic Diseases , released in 2002-3, also blamed high consumption of sugars for increasing prevalence of obesity and other chronic diseases.[50] But this report was rejected by the US govt., presumably under pressure from the sugar industry.[51,52]

The pathophysiological basis for the role of sugar in the development of modern diseases is also getting clearer. It is increasingly becoming clear that sugar, particularly fructose, plays a major role in the pathogenesis of modern diseases. Fructose increases de novo lipogenesis and induces dyslipidemia. Sugar being the source of alcohol, behaves like alcohol on the liver and on the brain, increases hunger and decreases satiety, and is more addicting than cocaine.[53-56] Sugar drives metabolic syndrome by increasing lipogenesis, increasing uric acid, reducing nitric oxide, increasing insulin resistance, increasing leptin resistance in the liver and increasing inflammation.[55,57] Carbohydrate, directly or indirectly through the effect of insulin, controls the disposition of excess dietary nutrients. Dietary carbohydrate modulates lipolysis, lipoprotein assembly and processing and affects the relation between dietary intake of saturated fat intake and circulating levels. Glucose and insulin operate through a collection of transcription factors to partition lipids toward anabolic pathways. Abnormal fatty acid metabolism and dyslipidemia, in turn, play an intimate role in the pathogenesis of metabolic syndrome and cardiovascular diseases.[39,58]

While the evidence against sugars is mounting, study after study has failed to prove a causal role for dietary fats in chronic diseases. Framingham study, WHI and many other studies, failed to show an association between dietary lipids and risk for cardiovascular disease (CVD), and also failed to show benefits for omega 6 polyunsaturated fats.[39,59-65] A systematic review of 32 observational studies (512 420 participants) of fatty acids from dietary intake and 17 observational studies (25 721 participants) of fatty acid biomarkers and 27 randomized, controlled trials (105 085 participants) of fatty acid supplementation 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.[66]

Studies have also absolved cholesterol from all the blame. Nord-Trøndelag Health Study (HUNT 2, 1995–1997) comprising 52 087 Norwegians, aged 20–74, who were followed-up on cause-specific mortality for 10 years (510 297 person-years in total) did not find any evidence against cholesterol and concluded that clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised, especially for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but even beneficial.[67]

The prospective, population-based Kuopio Ischaemic Heart Disease Risk Factor Study that included 1032 men aged 42–60 y in 1984–1989 found that egg or cholesterol intakes were not associated with the risk of CAD and also not associated with increased common carotid artery intima-media thickness.[1]

To cap it all, recovery and analysis of previously unpublished data from the Minnesota Coronary Experiment (MCE), from the seat of origin of the traditional diet-heart hypothesis, has disapproved the hypothesis itself. The MCE (1968-73) was a double blind randomized controlled trial designed to test whether replacement of saturated fat with vegetable oil rich in linoleic acid reduced coronary heart disease and death by lowering serum cholesterol. Recovered MCE unpublished documents and raw data, comprising of 9423 women and men aged 20-97, longitudinal data on serum cholesterol for the 2355 participants exposed to the study diets for a year or more and 149 completed autopsy files, were analyzed according to hypotheses prespecified by original investigators. Further, a systematic review and meta-analyses of randomized controlled trials that lowered serum cholesterol by providing vegetable oil rich in linoleic acid in place of saturated fat without confounding by concomitant interventions was conducted. Although the intervention group had significant reduction in serum cholesterol compared with controls (mean change from baseline −13.8% v −1.0%; P<0.001), there was no mortality benefit for the intervention group in the full randomized cohort or for any prespecified subgroup. There was a 22% higher risk of death for each 30 mg/dL (0.78 mmol/L) reduction in serum cholesterol in covariate adjusted Cox regression models (hazard ratio 1.22, 95% confidence interval 1.14 to 1.32; P<0.001). There was no evidence of benefit in the intervention group for coronary atherosclerosis or myocardial infarcts. Systematic review identified five randomized controlled trials for inclusion (n=10 808). In meta-analyses, these cholesterol lowering interventions showed no evidence of benefit on mortality from coronary heart disease (1.13, 0.83 to 1.54) or all cause mortality (1.07, 0.90 to 1.27). The authors concluded that available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes and that findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.[2]

Another systematic review identified 19 cohort studies including 30 cohorts with a total of 68094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found. The authors concluded that high LDL-C is inversely associated with mortality in most people over 60 years, a finding inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic), questioning the validity of the cholesterol hypothesis. The authors suggested a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.[4]

Many studies have now shown that low carb diets are better than low fat diets in preventing and managing modern diseases. Restriction of carbohydrates has been reported to reverse metabolic syndrome. A carbohydrate restricted diet corrects hyperglycemia, reduces triglycerides, LDL and increases HDL, reduces uric acid, reduces blood pressure, reduces weight and also corrects PCOS.[58] It is interesting to note that human beings do not need any carbohydrate intake for survival! The theoretical minimal level of carbohydrate intake is zero. Protein deprivation leads to kwashiorkor, and energy deprivation leads to marasmus; however, there is no specific carbohydrate deficiency syndrome and carbs are NOT listed as ESSENTIAL nutrients and there is no Recommended Daily Requirement.[68] Aboriginal hunting and fishing cultures, such as Inuit of the Arctic and First Nations groups in Canada, survived for millennia with little if any identifiable dietary carbohydrate intake. Hunter gatherers, who consumed 32% plant foods and 68% animal foods, were relatively free of the signs and symptoms of CVD and hunter gatherers also have low insulin levels.[58,69-71] It is to be noted that food staples and food-processing procedures introduced during the neolithic and industrial periods have fundamentally altered 7 crucial nutritional characteristics of ancestral hominin diets: 1) glycemic load, 2) fatty acid composition, 3) macronutrient composition, 4) micronutrient density, 5) acid-base balance, 6) sodium-potassium ratio, and 7) fiber content.[72] From the time of Australopithecus africanus, through the evolution of true hominids, up to and beyond Pithecanthropus, Neanderthal, and Cro-Magnon, man and his immediate ancestors have continued to be hunters, predators, anti scavengers, seeking their favorite food of meat and offal. With science and technology, man could separate palatability and nutrition, choosing the former over the latter and as result, in England alone, the consumption of sugar rose from 10,000 tons in 1700 to 150,000 tons by 1800.[22]

The Dietary Guidlines for Americans, which since 1980 recommended the restriction of dietary cholesterol to <300mg per day, has withdrawn such advice in 2015-16. The Scientific Report of the 2015 Dietary Guidelines Advisory Committee explicitly stated: Previously, the Dietary Guidelines for Americans recommended that cholesterol intake be limited to no more than 300 mg/day. The 2015 DGAC will not bring forward this recommendation because available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum cholesterol.. Cholesterol is not a nutrient of concern for overconsumption.[34] The 2015–2020 Dietary Guidelines for Americans has indeed dropped that recommendation.[73] Is it not time to switch over to our ancestral diet?

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Milk and Calcium

Milk and Calcium

Breastfeeding is nectar for the newborn; breast milk should be the exclusive feed for the first six months of life. But consumption of animal milk later in life does no good to our body and may even cause harm. Supplementation of calcium also can be detrimental; it has been reported to increase the risks of vascular events.

Emerging evidence:

Leptin and Diseases

Leptin and Diseases

Leptin is the hormonal signal from fat, the energy store, to our brain. Many functions of our body, like growth and development, energy expenditure, bone health, reproduction etc., are influenced by leptin. Thus leptin is the link that connects our body functions to our food and our energy stores. Excessive production of leptin leads to leptin resistance that in turn can lead to abnormal functioning of all these systems.

Emerging Evidence

  • Leptin, leptin receptors, and the control of body weight. Friedman JM. Nutr Rev. 1998 Feb;56(2 Pt 2):s38-46; discussion s54-75. [See]
  • Selective leptin resistance: a new concept in leptin physiology with cardiovascular implications. Mark AL et al. J Hypertension. 2002;20(7):1245-1250.[See]
  • Obesity in the new millennium. Friedman JM.[See]
  • Etiology of the Metabolic Syndrome: Potential Role of Insulin Resistance, Leptin Resistance, and Other Players. Zimmet P et al. Ann NY Acad Scs 1999;892:25-44. [See]
  • The Metabolic Significance of Leptin in Humans: Gender-Based Differences in Relationship to Adiposity, Insulin Sensitivity, and Energy Expenditure.  Kennedy et al. J Clin Endo Met. 1997;82(4):1293-1300. [See]
  • Obesity, Body Fat Distribution, Insulin Sensitivity and Islet b -Cell Function as Explanations for Metabolic Diversity. Kahn SE et al. J Nutr. 2001;131:354S-360S. [See]
  • Adipocytokines and Insulin Resistance. Pittas AG, Joseph NA, Greenberg AS. JCEM 89(2)447-452. [See]
  • Abdominal obesity and metabolic syndrome. Després JP, Lemieux I. Nature 2006;444:881-888. [See]
  • Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk. Després JP et al. Arteriosclerosis, Thrombosis, and Vascular Biology. 2008; 28: 1039-1049. [See]
  • Leptin mediates a proliferative response in human MCF7 breast cancer cells. Dieudonne MN et al. Biochemical and Biophysical Research Communications. 2002;293(1):622-628(7). [See]
  • Leptin is Associated with Increased Prostate Cancer Risk: A Nested Case-Referent Study.  Stattin P.JCEM. 86(3):1341-1345, [See]
  • Leptin and prostate cancer.  Chang S et al. Prostate. 2001;46(1):62-67. [See]
  • Leptin enhances, via AP-1, expression of aromatase in the MCF-7 cell line. Catalano S et al. J Biol Chem. 2003;278(31):28668-76. [See]
  • Association between Serum Leptin Concentrations and Bone Mineral Density, and Biochemical Markers of Bone Turnover in Adult Men. Sato M et al. JCEM 86(11):5273-5276. [See]
  • Leptin is Inversely Related to Age at Menarche in Human Females. Matkovic V et al. JCEM 1997;82(10):3239-3245. [See]
  • Role of obesity and leptin in the pubertal process and pubertal growth—a review. Shalitin S, Phillip M. International Journal of Obesity. 2003;27:869–874. doi:10.1038/sj.ijo.0802328 [See]
  • Link Between Body Fat and the Timing of Puberty. Kaplowitz PB. Pediatrics. 2008;121;S208. [See]
  • Are circulating leptin and luteinizing hormone synchronized in patients with polycystic ovary syndrome? Petermann TS et al. Hum Repro 1999;14(6):1435-1439. [See]
  • Overweight Kids Risk Weak Bones, Diabetes: Abdominal Fat May Play a Role in Bone Strength. Norman K Pollock et al. Lower bone mass in prepubertal overweight children with pre-diabetes Journal of Bone and Mineral Research Jul 2010 Abstract | Report]

Diet and Skin

Diet and Skin

Several skin diseases, especially acne, psoriasis, dandruff, vitiligo, hirsutism, male pattern baldness etc., are increasingly being associated with metabolic syndrome and with certain specific dietary patterns. There is evidence to show that dietary modifications can help in alleviating or preventing many of these problems.

New Evidence for Diet and Skin Diseases

  • Insulin Resistance and Skin Diseases. Napolitano M et al. The Scientific World Journal. Volume 2015, Article ID 479354, 11 pages
  • More than skin deep: dyslipidemia in skin diseases. Dreiher J, Cohen A. Clinical Lipidology. 2009;4(5):533-536
  • Dyslipidemia and metabolic syndrome in patients with lichen planus: A case-control study. Kuntoji V et al. Journal of Pakistan Association of Dermatologists. 2016;26 (4):290-297.
  • Lichen planus and dyslipidaemia: a case-control study. Dreiher J et al. Br J Dermatol. 2009 Sep;161(3):626-9. doi: 10.1111/j.1365-2133.2009.09235.x. Epub 2009 May 12.
  • Metabolic Derangements in Lichen Planus – A Case Control Study. Kar BR et al. Journal of Clinical and Diagnostic Research. 2016 Nov, Vol-10(11): WC01-WC03
  • Incidence of diabetes mellitus in patients with oral lichen planus. Lundström IM. International Journal of Oral Surgery. June 1983;12(3):147-152
  • High prevalence of glucose metabolism disturbance in patients with lichen planus. Seyhan M et al. Diabetes Research and Clinical Practice August 2007;77(2):198-202
  • Prevalence of Metabolic Syndrome in Patients with Mucosal Lichen Planus: A Case-Control Study. Baykal L et al. Am J Clin Dermatol. 2015 Oct;16(5):439-45.
  • Disturbance in glucose metabolism in patients of lichen planus. Zakaria ASM, et al. Banganandhu Sheikh Mujib Med Univ J. 1016;9:177
  • Serum Leptin and Lipid Profile in Lichen Planus: A Case Control Study. Sarkar M et al. International Journal of Health Sciences & Research October 2015;5(10):129
  • Cardiovascular Risk Factors in Patients with Lichen Planus. Arias-Santiago S et al. The American Journal of Medicine. June 2011;124(6):543-548
  • Lipid levels in patients with lichen planus: a case-control study. Arias-Santiago S et al. J Eur Acad Dermatol Venereol. 2011 Dec;25(12):1398-401.
  • Insulin Resistance is Increased in Patients with Vitiligo. Karadag AS et al. Acta Derm Venereol 2011; 91: 541–544
  • Increased Risk of Metabolic Syndrome in Patients with Vitiligo. Ataş H et al. Balkan Med J 2017;34:219-25 Original Article 219
  • Metabolic syndrome in Egyptian patients with vitiligo: a case–control study. Manara S et al. Journal of the Egyptian Women’s Dermatologic Society: May 2017;14(2):100–105
  • The relationship between rosacea and insulin resistance and metabolic syndrome. Akin BA. Eur J Dermatol. 2016 Jun 1;26(3):260-4. doi: 10.1684/ejd.2016.2748.
  • Metabolic Syndrome and Skin: Psoriasis and Beyond. Padhi T et al. Indian Journal of Dermatology 2013; 58(4) 299
  • Psoriasis and cardiovascular risk: Immune-mediated crosstalk between metabolic, vascular and autoimmune inflammation. Frers RAK et al. IJC Metabolic & Endocrine. March 2015;6:43-54 [Full Text]
  • Dietary implications for the development of acne: a shifting paradigm.  Cordain L.  In: U.S. Dermatology Review II 2006, (Ed.,Bedlow, J). Touch Briefings Publications, London, 2006.  [See]
  • Acne Vulgaris: A Disease of Western Civilization. Cordain L. Arch Dermatol. 2002;138:1584-1590. [See]
  • Evidence to link psoriasis with metabolic syndrome: Several reports in the recent years have suggested associations between psoriasis and metabolic syndrome sidorders. Results of a new study at Reykjavik’s Landspitali, the National University hospital of Iceland suggest that patients — especially women — with psoriasis may be at increased risk for metabolic syndrome. The study involving more than 6,500 people found the prevalence of metabolic syndrome to be higher among patients with psoriasis (40 percent) than among those without (23 percent) [See Love TJ et al. Prevalence of the Metabolic Syndrome in Psoriasis. Arch Dermatol. Published online December 20, 2010. doi:10.1001/archdermatol.2010.370. Abstract | Report]
  • Psoriasis and the Metabolic Syndrome. Cohen AD. Acta Derm Venereol 2007;87:506–509. Full Text
  • Psoriasis and the Metabolic Syndrome. Gottlieb AB et al. Journal of Drugs in Dermatology. June, 2008. Full Text
  • Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis Sommer DM et al. Arch Derm Res. 2006;298(7):321-328. Abstract
  • A study reported at the Society for Investigative Dermatology meeting suggested that severe psoriasis doubled the likelihood of metabolic syndrome as compared with no history of psoriasis and the the prevalence of each component of metabolic syndrome increased with psoriasis severity, including obesity, hypertriglyceridemia, and elevated glucose [Report]

Eggs and Meat

Eggs and Meat

Eggs have been blamed for increase in blood cholesterol, heart attacks, obesity etc. But on the contrary, there is enough evidence to show that eggs are safe and healthy. There appears to be no association between egg consumption and increase in blood cholesterol or the incidence of heart attacks. Eggs, in fact, make a good breakfast!

Emerging Evidence

Metabolic Syndrome

Metabolic Syndrome

Many modern day diseases such as obesity, type 2 diabetes, cardiovascular disease, lipid abnormalities, hypertension, PCOS, cancers, autoimmune diseases etc., are on the rise and striking younger population. Some of these have been clustered together as Metabolic Syndrome. Hyperinsulinemia and insulin resistance, hyperleptinemia and leptin resistance are at the core of these disorders.

Emerging Evidence

  • Binge Eating More Likely to Lead to Metabolic Syndrome in Men [Abstract | Report]
  • Liver, insulin and obesity [See]
  • Obesity and Metabolic Syndrome associated with Impaired Brain Function in Adolescents [See Pediatrics | Report | Report]
  • Diet Alone or With Exercise Improves Metabolic Syndrome. Nancy A. Melville for Medscape [See]
  • Metabolic Syndrome May be Due to Disease Causing Fat Cells: UC Davis Health System researchers have reported a novel observation that subcutaneous fat of MetS has increased macrophage recruitment with cardinal crown-like structure features and contributes to the increased cellular inflammation that produces increased levels of biomarkers that are correlated with both insulin resistance and low-grade inflammation. [Bremer AA et al. Adipose Tissue Dysregulation in Patients with Metabolic Syndrome. The Journal of Clinical Endocrinology & Metabolism August 24, 2011 jc.2011-1577. Abstract | Report]
  • Metabolic Syndrome Increases Risk of Kidney Disease: MetS and its components are associated with the development of eGFR <60 ml/min per 1.73 m2 and microalbuminuria or overt proteinuria, a meta analysis shows. [Thomas G et al. Metabolic Syndrome and Kidney Disease: A Systematic Review and Meta-analysis. CJASN August 2011 CJN.02180311.Abstract]
  • Metabolic Syndrome Increases Risk of Open Angle Glaucoma: Components of metabolic syndrome, including diabetes mellitus and systemic arterial hypertension, either alone or in combination, are associated with higher risk of open-angle glaucoma. [Newman-Casey PA et al. The Relationship Between Components of Metabolic Syndrome and Open-Angle Glaucoma. Ophthalmology July 2011;118(7):1318-1326. Abstract]
  • Metabolic syndrome increases kidney stone risk: Data from 34,895 individuals who underwent general health screening tests has revealed that kidney stones were 25% more likely to be found in subjects with metabolic syndrome than in those without it and that kidney stones were 47% more likely to be found in subjects with hypertension than in those without it. [In Gab Jeong et al. Association Between Metabolic Syndrome and the Presence of Kidney Stones in a Screened Population. AJKD. Article in press. Abstract]
  • Metabolic Syndrome and GERD linked: Gastroesophageal reflux disease (GERD), has a strong correlation with risk of metabolic syndrome, according to a cross-sectional study conducted in 100 patients. In the study, 50% of those with elevated 24-hour acid levels versus 20% of those without pathologically elevated acid, had metabolic syndrome. [See Report | Earlier Reports: Park JH et al.Metabolic syndrome is associated with erosive esophagitis World J Gastroenterol. 2008;14(35):5442–5447. | Kallel L. Metabolic syndrome is associated with gastroesophageal reflux disease based on a 24-hour ambulatory pH monitoring. Diseases of the Esophagus April 2011;24(3):153–159./a> | Ierardi E et al. Metabolic syndrome and gastro-esophageal reflux: A link towards a growing interest in developed countries. World J Gastrointest Pathophysiol. 2010;1(3):91-96. Chung SJ. Oesophagus Metabolic syndrome and visceral obesity as risk factors for reflux oesophagitis: a cross-sectional case–control study of 7078 Koreans undergoing health check-ups. Gut2008;57:1360-1365. | Lee Y-C. The effect of metabolic risk factors on the natural course of gastro-oesophageal reflux disease Gut 2009;58:174-181]
  • Improved outcomes associated with metformin therapy in patients with diabetes and heart failure: A two year follow-up study has found that metformin use in ambulatory patients with diabetes and heart failure improves outcome, contrary to what was believed. [David Aguilar et al. Metformin Use and Mortality in Ambulatory Patients with Diabetes and Heart Failure CIRCHEARTFAILURE.110.952556 October 15, 2010. doi: 10.1161/CIRCHEARTFAILURE.110.952556 Abstract | Report]
  • Apple Or Pear-Shaped Body Type Equally Dangerous: A study of 220,000 people suggests that being obese – having a body mass index (BMI) of 30 or more – is a major risk factor for heart disease, but found the distribution of fat on the body has no impact on that risk. [The Emerging Risk Factors Collaboration Separate and combined associations of body-mass index and abdominal adiposity with cardiovascular disease: collaborative analysis of 58 prospective studies. The Lancet. 11 March 2011. doi:10.1016/S0140-6736(11)60105-0 Full Text | Report]
  • Metabolic Syndrome Increases Age Related Memory Loss: A French study reports that several components of metabolic syndrome may be associated with age related cognitive decline [Abstract – Neurology February 8, 2011 vol. 76 no. 6 518-525]
  • Imbalanced diet and inadequate exercise may underlie asthma in children: Metabolic syndrome markers correlate with asthma, new study reveals. [See Report]
  • Chronic exposures to Bisphenol A, widely used in epoxy resins lining food and beverage containers, may lead to diabetes and cardiovascular events. See Full Text Article in JAMA | Report
  • More than half of the world’s population is overweight: See Report
  • Five Stages of Evolving Beta-Cell Dysfunction During Progression to Diabetes. Weir GC, Weir SB. Diabetes. 2004;53:S16-S21. [See]
  • Homocysteine and reactive oxygen species in metabolic syndrome, type 2 diabetes mellitus, and atheroscleropathy: The pleiotropic effects of folate supplementation. Hayden MR, Tyagi SC. Nutrition Journal 2004;3:4. [See]
  • High-Sensitivity C-Reactive Protein in Patients with Metabolic Syndrome. Guven A et al. Angiology. 2006:57(3):295-302. [See]
  • The Metabolic Syndrome and Concentrations of C-Reactive Protein Among U.S. Youth.  Ford ES et al. Diabetes Care 2005;28:878-881. [See]
  • Metabolic origins and clinical significance of LDL heterogeneity. Berneis KK, Krauss RM. J Lipid Res. 2002;43:1363-1379. [See]
  • Childhood Obesity Alone May Increase Risk of Later Cardiovascular Disease: Being obese by as early as 7 years of age may raise a child’s risk of future heart disease and stroke, even in the absence of other cardiovascular risk factors such as high blood pressure, according to a new study accepted for publication in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM). Abstract | Report in Science Daily |Report in Modern Medicine
  • Premature Death Awaits Obese Kids: Paul W. Franks et al., New Eng Journal Med., 11 February 2010 | Business Week Report
  • Reduction of body fat more important than fitness in lowering blood pressure: Individuals who have a healthy body weight are more likely than those who are physically fit to have lower blood pressure, shows a new study [Chen J, Das S, Barlow CE, Grundy S, Lakoski SG. Fitness, fatness, and systolic blood pressure: data from the Cooper Center Longitudinal Study. Am Heart J. 2010 Jul;160(1):166-70.] [Abstract] | Report]
  • Inflammation and insulin resistance. Carl de Luca, Jerrold M. Olefsky FEBS Letters. January 2008;582(1):97-105, 9. [See]
  • From individual risk factors and the metabolic syndrome to global cardiometabolic risk. Jean-Pierre Després et al. Eur Heart J Suppl March 2008;10 (suppl B):B24-B33. doi: 10.1093/eurheartj/sum041 [See]
  • The metabolic syndrome: common origins of a multifactorial disorder. Bruce KD, Byrne CD. Postgrad Med J 2009;85:614-621 doi:10.1136/pgmj.2008.078014 [See]
  • FROM MICE TO MEN: Insights into the Insulin Resistance Syndromes. Sudha B. Biddinger, Ronald Kahn C. Annual Review of Physiology. March 2006;68:123-158. DOI: 10.1146/annurev.physiol.68.040104.124723. [See]

Miscellaneous:

Salt and Disease

Salt and Disease

Increased consumption of salt, or sodium chloride, in our food has for long been considered as a risk factor for the development of vascular diseases and hypertension. Restriction of salt can help in the prevention of these maladies.

Emerging Evidence

Diet and Neuro-Mental Health

Diet and Neuro-Mental Health

Increasing evidence shows that diet plays an important role in the development of mental disorders such as neuroses, psychoses, ADHD etc., and nuerological disorders such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis etc.

Emerging Evidence

  • ‘Metabolic syndrome’ in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition. Rahul Agrawal, Fernando Gomez-Pinilla. The Journal of Physiology. May 1, 2012;590:2485-2499. doi: 10.1113/jphysiol.2012.230078. [Full Text] [UCLA Press Release]
  • Diet is linked to mental health: Jacka FN, Kremer PJ, Berk M, de Silva-Sanigorski AM, Moodie M, et al. A Prospective Study of Diet Quality and Mental Health in Adolescents. PLoS ONE 2011;6(9):e24805. doi:10.1371/journal.pone.0024805 [Full Text] | Felice N. Jacka et al. The Association Between Habitual Diet Quality and the Common Mental Disorders in Community-Dwelling Adults: The Hordaland Health Study
    Psychosomatic Medicine July 2011;73(6):483-490 [Abstract]
  • Eating nuts may enhance mood. [See]
  • ADHD is Associated With a ‘Western’ Dietary Pattern in Adolescents, Australian Study Finds The study involving 1,799 adolescents on 14-year follow-up has found that a diet high in the Western pattern of foods was associated with more than double the risk of having an ADHD diagnosis compared with a diet low in the Western pattern, after adjusting for numerous other social and family influences [Howard AL et al. ADHD Is Associated With a ‘Western’ Dietary Pattern in Adolescents. Journal of Attention Disorders, 2010; DOI: 10.1177/1087054710365990. Abstract | Report]
  • Fish Oil May Reduce Psychosis in High-Risk Individuals: G. Paul Amminger et al., Arch Gen Psychiatry February 2010 | Report
  • Maternal Metabolic Problems may Increase the Risk of Neurodevelopmental Problems, Including Autism, in Children: A population-based, case-control investigation between January 2003 and June 2010 at University of California, Davis, California, named CHARGE (Childhood Autism Risks from Genetics and the Environment) study, that enrolled hildren aged 2 to 5 years (517 autism spectrum disorder (ASD), 172 developmental delays (DD) and 315 controls) found that maternal metabolic conditions such as obesity and type 2 diabetes are a risk factor for autism, developmental delay without autistic symptoms, and impairments in several domains of development, particularly expressive language, after adjusting for sociodemographic and other characteristics. [Krakowiak P, Walker CK, Bremer AA, Baker AS, Ozonoff S, Hansen RL, Hertz-PicciottoMaternal I. Metabolic Conditions and Risk for Autism and Other Neurodevelopmental Disorders. Pediatrics 2011-2583; Published online April 9, 2012 (10.1542/peds.2011-2583) Full Text | Report
  • Berries may prevent Alzheimer’s disease: Eating blueberries, blackberries, strawberries may prevent cognitive decline, study finds. Miller MG, Shukitt-Hale B. Berry Fruit Enhances Beneficial Signaling in the Brain. J. Agric. Food Chem. DOI: 10.1021/jf2036033[Abstract Report]
  • Diet and Obesity May be Linked to Alzheimer’s: A Swedish study that included 8,534 twins over the age of 65, has found that the risk of dementia was almost double in those who were overweight versus those of normal weight and those who were obese had almost a fourfold increase in risk. [Johansson K at al. Longer term effects of very low energy diet on obstructive sleep apnoea in cohort derived from randomised controlled trial: prospective observational follow-up study BMJ 2011; 342:d3017  Abstract | Report | Older Paper]

Problem of Insulin

Problem of Insulin

High blood levels of insulin and resultant insulin resistance are identified to be at the root of several disorders, collectively called as Metabolic Syndrome. Both endogenous insulin and exogenous insulin, injected for treating diabetes mellitus, can cause problems. Keep your insulin levels low.

Emerging Evidence

  • Insulin causes more deaths than high blood glucose: ACCORD Study Finds
    Full Text of ACCORD Study in NEJM 2008;358(24):2545-2559 | Full Text of the Editorial in NEJM 2008;358(24):2630-2633 | Diabetes & Obesity: Why Conventional Medicine Makes Things Worse By Mark Hyman in Huffingtonpost.com
  • Survival as a function of HbA1c in people with type 2 diabetes: a retrospective cohort study Like the ACCORD Study, one more British study involving 47970 diabetics above the age of 50 years finds that low and high mean HbA1c values are associated with increased all-cause mortality and cardiac events, meaning that both uncontrolled disease as well as intensive treatment can kill. Craig J Currie et al., The Lancet, Early Online Publication, 27 January 2010
  • Sulfonylureas and insulin increase the risk of pancreatic cancer: A case–control study of general practice patients in the United Kingdom suggests that the use of antidiabetics such as sulfonylureas and insulin is associated with an increased risk for pancreatic carcinogenesis. Bodmer M, Becker C, Meier C, Jick SS, Meier CR. Use of Antidiabetic Agents and the Risk of Pancreatic Cancer: A Case–Control Analysis. The American Journal of Gastroenterology. 31 January 2012; doi:10.1038/ajg.2011.483[Abstract][Report][Report]
  • Most drugs for diabetes, except metformin, are not safe: A review of available treatment options for diabetes has found evidence to support metformin as a first-line agent to treat type 2 diabetes, whereas other options are associated with increased risk for hypoglycemia and other adverse events. [Bennett WL et al. Comparative Effectiveness and Safety of Medications for Type 2 Diabetes: An Update Including New Drugs and 2-Drug Combinations. Annals of Internal Medicine May 2011;154(9)602-613. Full Text | Report]
  • Higher Blood Sugar Increases Cancer Risk: Abnormal glucose metabolism, independent of BMI, is associated with an increased risk of cancer overall and at several cancer sites, with stronger associations among women than among men, and for fatal cancer compared to incident cancer Stocks T et al., Blood Glucose and Risk of Incident and Fatal Cancer in the Metabolic Syndrome and Cancer Project (Me-Can): Analysis of Six Prospective Cohorts. PLoS Med 2009;6(12): e1000201 | Report
  • Elevated Insulin Linked To Increased Breast Cancer Risk: ReportMoreMore
  • Insulin Induced Hypoglycemia Kills: Mark Santos, a 25-year-old truck driver, was killed when he apparently could not control the truck he was driving, resulting in a fatal crash. Jordan Santos, his brother, said that Mark was a diabetic who sometimes had trouble remembering what he did when his blood sugar levels were low. Mark was likely in a hypoglycemic state when he lost control of the vehicle, according to his brother See Video: http://video.aol.com/video-detail/canada-truck-crash/917237579
    The so called Human Insulin tends to cause hypoglycemia without warning and this tragic incident is a grim reminder of this fact. See Hypoglycemia and Human Insulin | Low blood sugar may impair diabetics’ driving: New Research Shows [See Full Text | Report]
  • Hyperinsulinemic diseases of civilization: more than just syndrome X [See]
  • Pathophysiology of Insulin Resistance and Noninsulin Resistance Dependent Diabetes [See]
  • Insulin and Its Metabolic Effects: Ron Rosedale [See]
  • Insulin Resistance Syndrome in Children. Ten S, Maclaren N. JCEM 89(6):2526-2539 [See]
  • Obesity, Insulin Resistance, Diabetes, and Cardiovascular Risk in Children. Circulation. 2003;107:1448. [See]
  • Insulin resistance syndrome (metabolic syndrome) and Asian Indians. Misra A, Vikram NK. Current Science 2002;83(12) [See]
  • Insulin through the ages: Phylogeny of a growth promoting and metabolic regulatory hormone. Chan SJ, Steiner DF.American Zoologist Apr 2000. [See]
  • Insulin: new roles for an ancient hormone. Ferrannini E et al. Eur J Clin Inv 1999;29(10):842-852(11) [See]
  • AMP-activated protein kinase – development of the energy sensor concept. Hardie DG, Hawley SA, Scott JW. J Physiol 574.1 pp 7-15. [See]
  • PPAR and human metabolic disease.Semple RK, Chatterjee VK, Rahilly SO. J. Clin. Invest. 2006;116:581-589. [See]
  • Insulin, Insulin-Like Growth Factors and Colon Cancer: A Review of the Evidence.  Giovannucci E. J. Nutr. 2001;131:3109S-3120S. [See]
  • Insulin resistance and breast-cancer risk.  Bruning PF et al. Int J Cancer. 1992;52(4):511-6. [See]
  • Glycemic index, hyperinsulinemia, and breast cancer risk. Key TJ. Annals of Oncology 2001;12:1507-1509. [See]
  • The Dietary Glycemic Index and its Implications in Cancer Risk, Insulin-Like Growth Factors and Oxidative Stress. Augustin LSA. University of Guelph. 2010. [See]
  • Dietary glycemic index and glycemic load, and breast cancer risk A case-control study.  Augustin LSA, Dal Maso L, La Vecchia C et al. Ann Oncol 2001;12:1533-1538. [See]
  • Diet, lifestyle, and colorectal cancer: is hyperinsulinemia the missing link? Kim YI. Nutr Rev. 1998;56(9):275-279. [See]
  • Metabolic syndrome affects breast cancer risk in postmenopausal women: National Cancer Institute of Naples experience. Capasso I et al. Cancer Biology & Therapy 2010;10(12):1240-1243. [See]
  • Nutrition, Insulin, Insulin-like Growth Factors and Cancer. Giovannucci E. Horm Metab Res 2003;35:694-704. [See]
  • Hyperinsulinemia in colon, stomach and breast cancer patients. Yam D et al. Cancer Lett. 1996;104(2):129-132. [See]
  • Insulin and colon cancer. Giovannucci E. Cancer Causes and Control 1995;6(2):164-179. [See]
  • Hyperinsulinemia in patients with colorectal cancer. Suehiro T et al. Hepatogastroenterology. 2005;52(61):76-78. [See]
  • Hyperinsulinemic diseases of civilization: more than just syndrome X.  Cordain L, Eades MR, Eades MD. Comp Biochem Physiol Part A. 2003;136:95-112. [See]
  • Metabolic Syndrome: Pathophysiology and Implications for Management of Cardiovascular Disease. Reaven G. Circulation. 2002;106:286. [See]
  • Insulin Resistance Syndrome. Rao G. American Family Physician. 2001;63(6). [See]
  • Obesity, Body Fat Distribution, Insulin Sensitivity and Islet -Cell Function as Explanations for Metabolic Diversity. Kahn SE et al. Journal of Nutrition. 2001;131:354S-360S. [See]
  • Insulin resistance and cardiovascular disease. Ginsberg HN. J Clin Inv. 2000;106(4):453-458. [See]
  • Effect of Intra-arterial Insulin on Tissue Cholesterol and Fatty Acids in Alloxan-Diabetic Dogs.  Cruz AB et al. Circulation Research. 1961;9:39. [See]
  • Insulin Causes Endothelial Dysfunction in Humans – Sites and Mechanisms.  Arcaro G et al. Circulation. 2002;105:576. [See]
  • Enhanced secretion of insulin plays a role in the development of atherosclerosis and restenosis of coronary arteries: elective percutaneous transluminal coronary angioplasty in patients with effort angina.  Nishimoto Y et al. J Am Coll Cardiol. 1998;32:1624-1629. [See]
  • Antihypertensive therapy and insulin sensitivity: do we have to redefine the role of beta-blocking agents? Jacob S, Rett K, Henriksen EJ. Am J Hypertens. 1998;11(10):1258-65. [See]
  • Hyperinsulinemia, insulin resistance, and the treatment of hypertension. Lithell HO. Am J Hypertens. 1996 Nov;9(11):150S-154S. [See]
  • Management of the metabolic syndrome.  Scheen AJ. Minerva Endocrinol. 2004 Jun;29(2):31-45. [See]
  • Glucose tolerance and insulin action in healthy centenarians. Paolisso G et al. Am J Physiol Endocrinol Metab 1996;270:E890-E894. [See]
  • Sex steroids and insulin resistance. Livingstone C, Collison M. Clinical Science. 2002;102:151–166. [See]
  • Exenatide, the new drug for diabetes, may cause pancreatitis: See Report

Sweet Poisons

Sweet Poisons

All that are sweet are poisonous. Sugar (Sucrose=Glucose+Fructose), Fructose (Fruit Sugar), artificial sweeteners – all these are toxic and are at the root of many of the modern day ills. Sweets increase hunger and cause craving, just like alcohol. The result: vicious spiral of metabolic abnormalities.

Here is the evidence

  • Sugar is Toxic: The growing scientific evidence, both epidemiological and mechanistic, very clearly shows that excess sugar induces all of the diseases associated with the metabolic syndrome, Robert H. Lustig et al write in Nature. See Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature. 02 February 2012;482:27–29. doi:10.1038/482027a[Link][Full Text][Report | Report | Report | Report]
  • ‘Metabolic syndrome’ in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition. Rahul Agrawal, Fernando Gomez-Pinilla. The Journal of Physiology. May 1, 2012;590:2485-2499. doi: 10.1113/jphysiol.2012.230078. [Full Text] [UCLA Press Release]
  • Sweetened Beverages Increase Coronary Heart Disease: de Koning L, Malik VS, Kellogg MD, Rimm EB, Willett WC, Hu FB. Sweetened Beverage Consumption, Incident Coronary Heart Disease and Biomarkers of Risk in Men. CIRCULATIONAHA.111.067017 doi: 10.1161/CIRCULATIONAHA.111.067017. [Full Text]
  • Sugar Consumption Increases Blood Pressure: The recently published INTERMAP study reveals that soft drinks, sweetened fruit juices, and sugar-loaded sports drinks are associated with significant increases in systolic and diastolic blood pressures. [Abstract from Brown IJ, Stamler J, Van Horn L, et al. Sugar-sweetened beverage, sugar intake of individuals and their blood pressure: INTERMAP study. Hypertension Feb 2011. doi: 10.1161/HYPERTENSIONAHA.110.165456 | Report]
  • Sweetened Beverages Increase Pancreatic Cancer Risk Mark A. Pereira et al. in Cancer Epidemiology, Biomarkers & Prevention, February 2010 Eva S. Schernhammer et al., in Cancer Epidemiology, Biomarkers & Prevention, Sep. 2005Report
  • Energy Drinks Pose Serious Health Risks for Young People: According to a review of scientific literature and Internet sources, published in Pediatrics, energy drinks that contain caffeine, taurine, sugars and sweeteners, herbal supplements etc., are regularly consumed by 30% to 50% of children, adolescents, and young adults and and are associated with risks for serious adverse health effects such as liver damage, kidney failure, respiratory disorders, agitation, confusion, seizures, psychotic conditions, nausea, vomiting, abdominal pain, rhabdomyolysis, tachycardia, cardiac dysrhythmias, hypertension, myocardial infarction, heart failure, and death. [See Seifert SM, Schaechter JL, Hershorin ER, Lipshultz SE. Health Effects of Energy Drinks on Children, Adolescents, and Young Adults. Pediatrics. 2011;127:511-528. DOI: 10.1542/peds.2009-3592. Free Full Text | Report]
  • Diet Soda and Salt Increase the Risk of Stroke: In a new study from the University of Miami’s Miller School of Medicine (Northern Manhattan Study), those who drink diet soda were found to have more than a 60% increase in stroke than those who abstain and those who used more than 4g of sodiun per day had double the risk than those who had less than 1.5g per day. Report | Report | Report]
  • Sugar sweetened beverages increase the risk of weight gain, development of metabolic syndrome and type 2 diabetes, meta analysis shows [See Malik VS et al. Sugar-Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes A meta-analysis. Diabetes Care November 2010;33(11):2477-2483 Free Full Text]
  • Sugar Sweetened Beverages Increase Diabetes Risk With or Without Weight Gain [See Full Text Diabetes CareReport]
  • Sugar Sweetened Beverages Increase the Risk of Metabolic Syndrome, Diabetes and Obesity Vasanti S. Malik et al. Sugar Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes: A Meta-analysis Diabetes Care. August 2010;33(8) Full Text | Report]
  • Television Watching and Soft Drink Consumption- Associations With Obesity in 11- to 13-Year-Old Schoolchildren. Giammattei J et al. Arch Pediatr Adolesc Med. 2003;157:882-886. [See]
  • Carbonated Soft Drink Consumption and Bone Mineral Density in Adolescence: The Northern Ireland Young Hearts Project. McGartland C et al. J Bone Miner Res 2003;18:1563–1569. [See]
  • Aspartame Disease: An FDA-approved Epidemic. Roberts HJ. [See]
  • Aspartame: A Safe Sweetener? Lawler H, Wylet L. [See]
  • Independent Analysis of the “Opinion of the European Commission, Scientific Committee on Food: Update on the Safety of Aspartame / E951. Gold MD. [See]

Fructose is Bad:

  • Dietary fructose linked to metabolic syndrome and diabetes mellitus: In a new study from Vanderbilt University in Nashville, Tennessee, a diet with 30 percent of total energy from fructose was given to 29 adult male rhesus monkeys aged 12 to 20 years for a period of 12 months. Starting at six months and by the end of the 12-month feeding study, ALL (100%) the monkeys developed certain metabolic syndrome components including body adiposity, insulin resistance, and dyslipidemia and four monkeys (15%) developed type 2 diabetes mellitus. [Bremer AA et al. Fructose-Fed Rhesus Monkeys: A Nonhuman Primate Model of Insulin Resistance, Metabolic Syndrome, and Type 2 Diabetes.Clinical and Translational Science. August 2011;4(4):243–252. Full Text | Report]
  • Increased fructose consumption from fruits increases metabolic syndrome risk: A cross-sectional population based study on 2537 subjects (45% men) aged 19-70 y has shown that higher consumption of dietary fructose may have adverse metabolic effects and increase the risks for metabolic syndrome. [Firoozeh Hosseini-Esfahani et al. Dietary fructose and risk of metabolic syndrome in adults: Tehran Lipid and Glucose study. Nutrition & Metabolism 2011, 8:50 doi:10.1186/1743-7075-8-50 Full text]
  • Certain Advanced Glycation End products (AGEs) Increase the risk of Complications in Diabetes: New study at the Joslin Diabetes Center has revealed that patients of Type 1 diabetes with higher levels of carboxyethyl-lysine and pentosidine AGEs are 7.2-fold more likely to have any complication. Earlier studies had revealed that these AGEs are linked more to fructose. [Sun JK et al. Protection From Retinopathy and Other Complications in Patients With Type 1 Diabetes of Extreme Duration: The Joslin 50-Year Medalist Study. Diabetes Care 29 March, 2011;34(4):968-974. doi: 10.2337/dc10-1675 Full Text | Mikulíková K, Eckhardt A, Kunes J, Zicha J, Miksík I. Advanced glycation end-product pentosidine accumulates in various tissues of rats with high fructose intake. Physiol Res. 2008;57(1):89-94. Epub 2007 Feb 8. Full text | Krajčovičova-Kudlačkova M, Šebekova K, Schinzel R, Klvanova J. Advanced Glycation End Products and Nutrition. Physiol. Res. 2002;51:313-316. Full text]
  • Glucose increases and fructose reduces brain activity: A functional brain magnetic resonance imaging (fMRI) study at Oregon Health and Science University has found that infusion of glucose enhances brain cortical activity but fructose infusion has the opposite effect, with reduced activity. While bigger studies are needed to confirm the findings, this may be one of the clues for patterns of our behaviour in general, and food consumption in particular. [Abstract from Purnell JQ et al. Brain functional magnetic resonance imaging response to glucose and fructose infusions in humans Diabetes, Obesity and Metabolism March 2011;13(3):229–234. |Report]
  • Fructose Worsens Gout: Consumption of soft drinks sweetened with sugar and fructose is strongly associated with an increased risk for gout, according to the results of a prospective cohort study reported in the February 1 Online First issue of the BMJ. This was a 12-year follow-up study of 46,393 health professionals without a previous history of gout and the goal was to assess the relationship between consumption of sugar-sweetened soft drinks and fructose and the risk for incident gout. See Sweet Soft Drinks, Fructose Linked to Increased Risk for Gout. Available at http://www.medscape.com/viewarticle/569656
  • Gout Linked to Increased Risk for Diabetes, Renal Disease [See]
  • High fructose intake in the form of added sugar is independently associated with higher blood pressure, according to the results of a cross-sectional analysis of data from the National Health and Nutrition Examination Survey [Diana I. Jalal, Gerard Smits, Richard J. Johnson and Michel Chonchol. Increased Fructose Associates with Elevated Blood Pressure. Journal of the American Society of Nephrology. July 1, 2010. doi: 10.1681/ASN.2009111111][Full text] | Report]

Fructose (Fruit Sugar) is a more important cause for metabolic disorders like diabetes, hypertension, fatty liver disease, obesity