Insulin Can Be Irresistible.

FriendlyBugs Although it’s an understatement to say many are recommending sugar restriction as a means to improving health, evidence – relating to inflammatory conditions like insulin resistance, obesity and diabetes – indicates that this approach is unsafe, and can end up becoming a powerful driver of worsening inflammation and disease.

A good way to understand how this might happen, is to look at how exposure to stress, in combination with lack of sugar availability, can inhibit metabolic function, and promote factors which increase biochemical stress. Many of these factors are central to the progression of the inflammatory blood sugar and insulin dysregulated conditions. Problems relating to digestion, tend to be more relevant than most realize.

“Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic patients…an important clue to link inflammation to the pathogenesis of type 2 diabetes (T2D), but the antihyperglycemic and antiinflammatory effects of salicylates were not connected to the pathogenesis of insulin resistance until recently…obesity, T2D, and CVD [cardiovascular disease] share a metabolic milieu characterized by insulin resistance and chronic subacute inflammation.” (Shoelson SE, et al., 2006)

“The present study examined the relationships between cortisol and related parameters of IR…possible pathophysiological mechanisms for the association between…stress and IR or diabetes involve hyper-stimulation of the HPA axis due to stress…chronic stress was associated with IR and may contribute to the development of IR.” (Yan YX, et al., 2016)

“Central to metabolic diseases is insulin resistance associated with a low-grade inflammatory status…we looked for a molecule involved early in the cascade of inflammation and identified LPS (bacterial endotoxin)…LPS is a strong stimulatory of the release of several cytokines that are key inducers of insulin resistance.” (Patrice D. Cani, et al., 2007)

When stress is high and sugar intake is restricted, glycogen stores are fast depleted, and the stress hormones, cortisol and adrenaline, will generally rise, as part of a process which is designed to provide alternative sources of fuel.

Adrenaline helps get the remaining glycogen out of storage and releases fat from tissue, in the form of free fatty acids. Cortisol breaks down muscle and other tissue, so that it can be used for the provision of more energy. The stress substances are crucial for survival, however when they are chronically or excessively raised, they promote degeneration and disease.

If the fatty acids released out of storage into circulation as a result of stress, are made up of high levels of the polyunsaturated fats (PUFAs), they can have a long term negative impact upon numerous biological processes, known to be involved in the progression of insulin related problems.

PUFAs and their breakdown products, are able to promote the development of a chronic inflammatory stress state, responsible for encouraging insulin dysfunction (and many related metabolic issues), in a manner which can become self-perpetuating, and difficult to reverse. The PUFAs are highly unstable, and can easily and rapidly break down inside the body.

“Oxidized derivatives of linoleic acid…may be involved in the increased glucocorticoid production observed in obese humans.” (Bruder ED, et al., 2003)

“Increased MDA [Malondialdehyde, breakdown product of PUFAs]…was a risk factor for non-alcoholic steatohepatitis…insulin resistance in NAFLD correlates with enhanced oxidative stress. Histopathological disease severity significantly correlated with oxidative stress parameters…” (Köroğlu E, et al., 2016)

“…lipogenic enzyme mRNAs were markedly reduced with increasing dietary corn oil in a dose dependent fashion…PUFA-mediated suppression of the mRNA…was partially restored by pioglitazone treatment…effects…seem to be due to increased insulin sensitivity.” (Iritani N, Fukuda H. 1995)

“Obesity is closely associated with insulin resistance and establishes the leading risk factor for type 2 diabetes mellitus…c-Jun amino-terminal kinases (JNKs) can interfere with insulin action…and are activated by inflammatory cytokines and free fatty acids, molecules…implicated in the development of type 2 diabetes.” (Hirosumi J, et al., 2002)

“…accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB.” (Mazière C, et al., 1999)

The greater the exposure to the stress promoting inflammatory byproducts of the degradation of PUFAs, the more this is likely to interfere with insulin function and proper blood sugar regulation. This then causes further stress, inflammation, and overall damage to metabolism. Intestinal bacterial issues are intertwined with these kinds of metabolic problems. Sugar is protective against stress. Salt and magnesium are also very important.

The byproducts of the PUFAs, stimulate the release of the stress substances (including cortisol, adrenaline, serotonin, nitric oxide and estrogen) and powerfully inhibit thyroid performance, suppressing mitochondrial energy metabolism. A slow metabolism, with increasing exposure to the PUFAs, tends to impede digestion. Sugar increases metabolism and inhibits polyunsaturated free fatty acid release.

A sub-optimal thyroid metabolism and digestive system, allows for bacteria to feed and grow in quantity, moving further up into the small intestine where it is not intended for them to be, promoting exposure to harmful and inflammatory bacterial toxins like endotoxin (LPS). Endotoxin causes serotonin production to be increased.

“…the gut microbiota plays a key role in promoting levels of colon and blood 5-HT (serotonin)…select microbes and their metabolic products can be used to promote endogenous, localized 5-HT biosynthesis…” (Yano JM, et al., 2015)

“…results further support the current view that the gut microbiota plays a crucial role in promoting the production of biologically active, free 5-HT.” (Hata T, et al., 2017)

Increased circulating serotonin levels, have been shown to be an important factor involved in the promotion of blood sugar dysregulation and insulin issues, which often lead to obesity and diabetes.

“Recent studies revealed that peripheral 5-HT [serotonin] plays an important role in metabolic regulation in peripheral tissues, where it suppresses adaptive thermogenesis in brown adipose tissue…suppressing 5-HT signaling might represent a new target for anti-obesity treatment by increasing energy expenditure and improving insulin resistance.” (Oh CM, et al., 2016)

“SERT-deficient mice exhibit hyperglycemia and insulin resistance, both of which are characteristic features of diabetes.” (Chen X, et al., 2012)

Serotonin and endotoxin, have both been demonstrated to promote inflammation, and to inhibit mitochondrial energy metabolism, leading to further stress and circulation of PUFAs, interfering with the proper use of sugar. Examining ways to improve digestion, in order to minimize bacterial issues, makes a lot of sense in the context of inflammatory conditions which rise under stress, and are associated with insulin resistance.

“Latest evidence suggests…bacterial LPS (endotoxin) deriving from the gut microbiota may trigger inflammation and oxidative stress in response to diets…This “metabolic endotoxemia” has been shown to initiate or promote obesity, insulin resistance, metabolic syndrome, and finally diabetes.”  (Pussinen PJ, et al., 2011)

“A striking inflammatory response is septic shock. We tested the hypothesis that non-neuronal serotonin enhances this neutrophil-driven disorder…Indeed, Tph1-/- mice were protected from lethal LPS-induced septic shock…The release of serotonin is yet another way by which platelets enhance inflammatory responses. Excessive neutrophil recruitment may thus also become a target of antiserotonergic treatment strategies.” (Duerschmied D, et al., 2013)

Contrary to popular beliefs, there is good evidence showing that rising serotonin is a central element involved in the progression of depression and anxiety. Endotoxin and inflammation are also closely connected to mental dysregulation, and depression, anxiety, and diabetes often go hand in hand.

“…endotoxaemia and inflammation owing to increased intestinal 5-HT may underpin the depression and diabetes association, where the risk of the latter pathology becomes particularly preeminent after the onset of depression…” (Pomytkin IA, et al., 2015)

Stress and lack of sugar, combined with mineral and nutrient deficiencies, and excessive exposure to PUFAs, can powerfully suppress thyroid energy metabolism and digestive function, also impacting upon intestinal barrier capabilities. Interference with the gut barrier, is more dangerous when bacterial issues exist, as more of the toxic bacterial byproducts, like endotoxin, have the opportunity to pass through to the liver. Serotonin excess has been shown to promote intestinal permeability.

If the liver becomes stressed and overloaded, this interferes with detoxification functions, which means that harmful substances produced in the intestine (such as bacterial endotoxin and serotonin) pass into the main system in greater quantities, where they promote further inflammation, aggravating problems associated with insulin function and diabetes. The combination of the PUFAs, high serotonin, and endotoxin, is inflammatory and anti-metabolic. Apart from their diabetogenic effects, all these things can be involved in the progression of nonalcoholic fatty liver disease (NAFLD), obesity, and heart disease.

“…high-fat feeding dramatically increased intestinal permeability…gut bacteria are involved in the control of intestinal permeability and furthermore in the occurrence of metabolic endotoxemia.” (Patrice D. Cani, et al., 2008)

“Compelling evidence supports the concepts that gut microbiota actively promotes weight gain and fat accumulation and sustains, indirectly, a condition of low-grade inflammation, thus enhancing the cardiovascular risk.” (Manco M, et al., 2010)

“Previous studies suggested that alterations in intestinal motility and permeability contribute to the development of NAFLD…treatment…caused a reduction of elevated serotonin levels… resulting in a reduction of endotoxin influx into the liver and subsequently of liver inflammation and fat accumulation.” (Haub S, et al., 2011)

The liver is responsible for preparing estrogen for excretion. Excess estrogen interferes with liver function, inhibits thyroid performance, and promotes serotonin levels, and these conditions can provoke stress and rising cortisol and adrenaline levels, and can encourage a general state of metabolic suppression, nervous system and immune dysfunction, and blood sugar dysregulation.

When stress and inflammation is high, estrogen is more likely to get trapped inside tissue. Actual levels of estrogen in the body, are not accurately reflected in blood test results, encouraging misleading (although very popular) ideas with regards to ‘estrogen deficiencies’ as a cause of illness, when it is excess estrogen that is the real problem. Prolactin (a substance which is connected to stress and inflammation), promotes cortisol release, and is associated with insulin resistance, and prolactin levels are known to be an accurate measure of tissue estrogen status.

As estrogen levels go up, and liver function is increasingly interfered with, thyroid hormone is less able to be converted into the metabolically active form (T3), further adding to stress and the suppression of energy system function, leading to greater release of the polyunsaturated free fatty acids, and worsening inflammation and insulin resistance.

Rising levels of endotoxin, serotonin, and estrogen, in combination with high levels of exposure to the PUFAs, seem to go together with rising stress, causing a worsening of inflammation and insulin resistance, and an exacerbation of bacterial issues. All this increases the occurrence of obesity, diabetes, and cardiovascular disease, and other inflammatory conditions.

“…evidence suggests that changes in intestinal microbial composition could be responsible for increased endotoxemia in response to a high-fat diet, which in turn would trigger the development of obesity and diabetes.” (Patrice D. Cani, et al., 2008)

“Experiments…have shown that endotoxin is associated with cardiometabolic abnormalities including obesity, insulin resistance, and diabetes….Importantly, a high-fat diet increased the proportion of…LPS-containing microbiota in the gut.” (Pussinen PJ, et al., 2011)

“In vivo experiments have demonstrated that injections of bacterial endotoxins induce systemic inflammation, which is accompanied by the appearance of insulin resistance…serum LPS [endotoxin] activity is inversely correlated with insulin sensitivity both in diabetic and nondiabetic cohorts.” (Lassenius MI, et al., 2011)

Bacterial endotoxin is directly inflammatory, and both endotoxin and inflammation can promote a rise in levels of the stress substance nitric oxide, which suppresses thyroid energy metabolism, and is another factor in the development of insulin resistance and related metabolic issues.

“Increased nitric oxide (NO) production, especially as a consequence of inducible nitric oxide synthase (iNOS), has also been implicated in insulin resistance, especially in the context of obesity…iNOS is markedly increased in macrophages and other inflammatory cells stimulated by proinflammatory cytokines.” (Evans JL, Goldfine ID., 2013)

“LPS [endotoxin] and the accompanying inflammatory stress markedly impair insulin stimulated muscle glucose uptake as well as induce cardiovascular dysfunction…an increase in NO availability alone in the absence of an inflammatory stress markedly impaired insulin-stimulated MGU [muscle glucose uptake]…” (Lawrence M. House II, et al., 2015)

“Considering the hyperactivity of the inducible NO synthase in MS [metabolic syndrome], these data confirm the altered redox and inflammatory status that characterizes the MS and suggest a link between lipid peroxidation, inflammation, and insulin resistance…examination…shows… in particular, a significant positive association between NOx and the degree of insulin resistance.” (Caimi G, et al., 2014)

Stress and the suppression of oxidative metabolism, causes lactate levels to go up, encouraging insulin resistance, and increasing diabetes risk. Lactate has also been shown to be a driver of cancer, and evidence suggests that high lactate is one of the reasons for the link between cancer and diabetes. Low blood sugar promotes lactate.

“Accumulative evidence indicates a high incidence and mortality for a variety of malignancies in patients with diabetes…Diabetes and cancer interact with each other in a vicious cycle, where lactate plays a pivotal role in this mutual interaction. Insulin resistance/diabetes and cancer conditions produce high levels of lactate and conversely high lactate promotes diabetes and cancer development and progression…” (Wu Y, et al., 2016)

Depending on individual metabolic circumstances, sugar restriction (especially when used to help with existing problems), can be just the thing needed to set in motion a cascade of interrelated, often synergistic, stressful, and inflammatory changes, popularly blamed on the consumption of too much sugar.

Lack of sugar increases cortisol, adrenaline, and free fatty acids, which inhibits thyroid function and digestion, promoting bacterial endotoxin. Endotoxin increases inflammation, and can cause estrogen, serotonin and nitric oxide to rise, stressing the liver. Low sugar also reduces liver function, allowing for systemic inflammatory issues to rise. Endotoxin, nitric oxide, serotonin, and estrogen, suppress oxidative metabolism, increasing lactate. These things promote each other, and further fuel the inflammatory response, increasing stress and insulin resistance, creating a self-feeding downward spiral. Stress and high cortisol from sugar restriction, magnifies the inflammatory response to endotoxin.

“…transient elevation of in vivo cortisol concentrations to levels that are observed during major systemic stress enhanced a subsequent, delayed in vivo inflammatory response to endotoxin. This appeared to be a dose-dependent effect that was more prominent at intermediate concentrations of cortisol than at higher concentrations of cortisol.” (Yeager MP, et al., 2009)

Carbohydrate consumption (in particular the difficult to digest starchy, fibrous foods) can also promote bacterial overgrowth and endotoxemia, although this is far more likely to be true in combination with consumption of PUFAs, when stress is high, when minerals and vitamins are deficient, and when metabolism and digestion are already less than optimal.

I’m not a doctor or a nutritionist, and this is not medical, health or dietary advice, but my experience has shown me that at times like this, it is even more important to experiment with ways to ensure that sugar and protein and other nutrients, can be supplied in a manner which is as easy as possible for digestion. High fat, high carb meals, especially those which are high in PUFAs and starches, can be inflammatory, and can add to bacterial, insulin, and blood sugar issues.

“HFHC (high PUFA high carb) meal…induces an increase in plasma LPS (endotoxin)…relevant to the pathogenesis of postprandial oxidative and inflammatory stress, insulin resistance, and atherosclerosis…” (Ghanim H, et al., 2009)

Orange juice – as well as white sugar, or sugar from fruit in general – with plenty of salt, can powerfully protect against stress, lowering exposure to endotoxin, estrogen, serotonin, nitric oxide, lactate, cortisol, and adrenaline. From this perspective, sugar can be seen as an anti-inflammatory, anti-diabetes, pro-metabolism food.

“The combination of glucose…and the HFHC meal induced oxidative and inflammatory stress and an increase in…endotoxin….orange juice intake with the HFHC meal prevented meal-induced oxidative and inflammatory stress…” (Ghanim H, et al., 2010)

It’s true that the consumption of any kind of fat can cause a temporary insulin resistant state, but it is the PUFAs which are known to stimulate chronic inflammation, and which can prevent the return to normal function, after stress is lowered or when sugar for fuel becomes available. One of the benefits of the highly saturated fats, like coconut oil for instance, is that they are anti-inflammatory, and have anti-bacterial properties.

“Our findings provide evidence for early biological adaptations to high fat feeding that proceed and possibly lead to insulin resistance…our study is the first to demonstrate that circulating endotoxin concentrations are increased following 5 days of an isocaloric, HFD [30% carbohydrate, 15% protein, and 55% fat (25% SFA)] in healthy humans.” (Anderson AS, et al., 2015)

Another possible advantage of a lower fat (and very low PUFAs), moderate protein, high carb diet, is that excess sugar will either be stored as glycogen for later use, or converted into predominantly saturated fats, which are anti-inflammatory, and can be used as fuel during times of stress, without causing harm to metabolism.

A diet avoiding the PUFAs, and with enough protein from milk, cheese, meat and gelatin, with plenty of sugar from easily digestible sweet ripe fruits, fruit juice, white sugar, and honey, is one way to help protect against stress, promote thyroid function and energy metabolism, and limit the blood sugar dysregulating, insulin interfering, inflammatory effects of excess exposure to endotoxin and other toxic things.

“Resistance to endotoxin in essential fatty acid-deficient (EFAD) rats is associated with reduced synthesis of certain arachidonic acid metabolites…Endotoxin caused a less severe change in permeability index in…EFAD (essential fatty acid deficient) rats than in normal rats…” (Li EJ, et al., 1990)

When enough sugar is provided (in the context of a nutrient/mineral dense, easy to digest diet) and stress is lowered, polyunsaturated fats still in storage, can be safely eliminated, leading to less exposure to the stress substances (including cortisol, serotonin, nitric oxide, estrogen and lactate). Together, this can allow for a gradual lowering of inflammatory issues, and an improvement in blood sugar regulation, and overall metabolic performance.

The ease of digestion of a pro-metabolic high sugar, high salt, low PUFAs diet, reduces stress, inhibits bacterial issues, improves gut barrier function, lowers endotoxin circulation, improves insulin sensitivity, and can protect against obesity, diabetes, heart disease, cancer, and metabolic issues in general. In this sense sugar is powerfully anti-bacterial, and not the villain it is made out to be.

“…gut bacteria are involved in…metabolic endotoxemia…inflammation, and metabolic disorders. This effect could be mediated by a mechanism that could increase gut permeability and enhance LPS absorption. Antibiotic treatment significantly lowers plasma LPS levels, gut permeability, and the occurrence of…inflammation, oxidative stress…and metabolic disorders.” (Patrice D. Cani, et al., 2008)

Some other things which are pro-metabolism and have the potential to protect against bacterial issues and improve insulin function, include magnesium, biotin, riboflavin, B6, coffee and caffeine, activated charcoal, coconut oil, niacinamide, thyroid hormone, aspirin, glycine, cascara, taurine, minocycline and some other antibiotics, certain antihistamines like cyproheptadine and famotidine, and pregnenolone.

The antibiotic, anti-microbial effects, of a daily raw carrot salad and some occasional well cooked mushrooms, can also help protect against bacterial overgrowth and related insulin dysregulating effects.

See more here

Diabetes Care. 2011 Feb;34(2):392-7. Endotoxemia Is Associated With an Increased Risk of Incident Diabetes. Pussinen PJ, Havulinna AS, Lehto M, Sundvall J, Salomaa V.

Diabetes. 2008 Jun;57(6):1470-81. Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice. Cani PD, Bibiloni R, Knauf C, Waget A, Neyrinck AM, Delzenne NM, Burcelin R.

Diabetes. 2007 Jul;56(7):1761-72. Metabolic Endotoxemia Initiates Obesity and Insulin Resistance. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmée E, Cousin B, Sulpice T, Chamontin B, Ferrières J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R.

Endocr Rev. 2010. Gut microbiota, lipopolysaccharides, and innate immunity in the pathogenesis of obesity and cardiovascular risk. Manco M, et al.

Med Hypotheses. 2008;71(1):45-52. Psychological stress, insulin resistance, inflammation and the assessment of heart disease risk. Time for a paradigm shift? Ware WR.

Circ Shock. 1990 Jun;31(2):159-70. Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability. Li EJ, Cook JA, Spicer KM, Wise WC, Rokach J, Halushka PV.

Proc Assoc Am Physicians. 1999 May-Jun;111(3):241-8. Review. Free fatty acids, insulin resistance, and type 2 diabetes mellitus. Boden G.

J Biol Chem. 2005 Oct 21;280(42):35361-71. JNK and tumor necrosis factor-alpha mediate free fatty acid-induced insulin resistance in 3T3-L1 adipocytes. Nguyen MT, Satoh H, Favelyukis S, Babendure JL, Imamura T, Sbodio JI, Zalevsky J, Dahiyat BI, Chi NW, Olefsky JM.

Amino Acids. 2012 May;42(5):1529-39. The potential usefulness of taurine on diabetes mellitus and its complications. Ito T, Schaffer SW, Azuma J.

Oxid Med Cell Longev. 2014;2014:824756. Lipid Peroxidation, Nitric Oxide Metabolites, and Their Ratio in a Group of Subjects with Metabolic Syndrome. Caimi G, Lo Presti R, Montana M, Noto D, Canino B, Averna MR, Hopps E.

Age (Dordr). 2013 Oct;35(5):1755-65. Chronic caffeine intake reverses age-induced insulin resistance in the rat: effect on skeletal muscle Glut4 transporters and AMPK activity. Guarino MP, Ribeiro MJ, Sacramento JF, Conde SV.

Behav Brain Res. 2015 Jan 1;276:111-7. Endotoxaemia resulting from decreased serotonin tranporter (5-HTT) function: a reciprocal risk factor for depression and insulin resistance? Pomytkin IA, Cline BH, Anthony DC, Steinbusch HW, Lesch KP, Strekalova T.

Diabetes Res Clin Pract. 2010 Dec;90(3):288-96. Taurine prevents free fatty acid-induced hepatic insulin resistance in association with inhibiting JNK1 activation and improving insulin signaling in vivo. Wu N, Lu Y, He B, Zhang Y, Lin J, Zhao S, Zhang W, Li Y, Han P.

Magnes Res. 2004 Jun;17(2):126-36. Review. Intracellular magnesium and insulin resistance. Takaya J, Higashino H, Kobayashi Y.

Pak J Biol Sci. 2010 Aug 1;13(15):723-30. Review. Lipid peroxidation alterations in type 2 diabetic patients. Marjani A.

Immunity. 2016 Apr 19;44(4):833-46. Human Monocytes Engage an Alternative Inflammasome Pathway. Gaidt MM, Ebert TS, Chauhan D, Schmidt T, Schmid-Burgk JL, Rapino F, Robertson AA, Cooper MA, Graf T, Hornung V.

J Pharmacol Exp Ther. 2011 Dec;339(3):790-8. Serotonin receptor type 3 antagonists improve obesity-associated fatty liver disease in mice. Haub S, Ritze Y, Ladel I, Saum K, Hubert A, Spruss A, Trautwein C, Bischoff SC.

Circ Shock. 1979;6(4):333-42. Resistance of essential fatty acid-deficient rats to endotoxic shock. Cook JA, Wise WC, Callihan CS.

PLoS One. 2010 Dec 28;5(12):e15912. Endotoxin Mediated-iNOS Induction Causes Insulin Resistance via ONOO− Induced Tyrosine Nitration of IRS-1 in Skeletal Muscle. Pilon G, Charbonneau A, White PJ, Dallaire P, Perreault M, Kapur S, Marette A.

Nature. 2002 Nov 21;420(6913):333-6. A central role for JNK in obesity and insulin resistance. Hirosumi J, Tuncman G, Chang L, Görgün CZ, Uysal KT, Maeda K, Karin M, Hotamisligil GS.

Am J Physiol Endocrinol Metab. 2002 Aug;283(2):E233-40. Lactate induces insulin resistance in skeletal muscle by suppressing glycolysis and impairing insulin signaling. Choi CS, Kim YB, Lee FN, Zabolotny JM, Kahn BB, Youn JH.

Diabetes Care. 2009 Dec;32(12):2281-7. Increase in Plasma Endotoxin Concentrations and the Expression of Toll-Like Receptors and Suppressor of Cytokine Signaling-3 in Mononuclear Cells After a High-Fat, High-Carbohydrate Meal. Ghanim H, Abuaysheh S, Sia CL, Korzeniewski K, Chaudhuri A, Fernandez-Real JM, Dandona P.

Pediatr Res. 2008 Oct;64(4):334-9. Attenuation of Lipopolysaccharide Induced Inflammatory Response and Phospholipids Metabolism at the Feto-Maternal Interface by N-Acetyl-Cysteine. Paintlia MK, Paintlia AS, Singh AK, Singh I.

Circ Shock. 1990 Jun;31(2):159-70. Resistance of essential fatty acid-deficient rats to endotoxin-induced increases in vascular permeability. Li EJ, Cook JA, Spicer KM, Wise WC, Rokach J, Halushka PV.

Eur Cytokine Netw. 2004 Apr-Jun;15(2):99-104. Prolactin triggers pro-inflammatory immune responses in peripheral immune cells. Brand JM, Frohn C, Cziupka K, Brockmann C, Kirchner H, Luhm J.

Biochem Biophys Res Commun. 1999 Nov;265(1):116-22. Cellular enrichment with polyunsaturated fatty acids induces an oxidative stress and activates the transcription factors AP1 and NFkappaB. Mazière C, Conte MA, Degonville J, Ali D, Mazière JC.

J Diabetes Res. 2015;2015:102054. Plasma Lactate Levels Increase during Hyperinsulinemic Euglycemic Clamp and Oral Glucose Tolerance Test. Berhane F, Fite A, Daboul N, Al-Janabi W, Msallaty Z, Caruso M, Lewis MK, Yi Z, Diamond MP, Abou-Samra AB, Seyoum B.

J Nutr Biochem. 2014 Jan;25(1):66-72. Nicotinamide improves glucose metabolism and affects the hepatic NAD-sirtuin pathway in a rodent model of obesity and type 2 diabetes. Yang SJ, Choi JM, Kim L, Park SE, Rhee EJ, Lee WY, Oh KW, Park SW, Park CY.

PLoS One. 2012;7(3):e32511. Reduced Serotonin Reuptake Transporter (SERT) Function Causes Insulin Resistance and Hepatic Steatosis Independent of Food Intake. Chen X, Margolis KJ, Gershon MD, Schwartz GJ, Sze JY.

The Journal of Clinical Endocrinology & Metabolism, Volume 38, Issue 5, 1 May 1974, Pages 836–840, Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine. JAMES W. PLONK, CARL H. BIVENS, JEROME M. FELDMAN.

Scientific Reports volume 5, Article number: 17192 (2015). Astaxanthin prevents and reverses diet-induced insulin resistance and steatohepatitis in mice: A comparison with vitamin E. Yinhua Ni, Mayumi Nagashimada, Fen Zhuge, Lili Zhan, Naoto Nagata, Akemi Tsutsui, Yasuni Nakanuma, Shuichi Kaneko & Tsuguhito Ota.

J Clin Endocrinol Metab. 2012 Jul;97(7):E1182-6. Skeletal Muscle Lipid Peroxidation and Insulin Resistance in Humans. Ingram KH, Hill H, Moellering DR, Hill BG, Lara-Castro C, Newcomer B, Brandon LJ, Ingalls CP, Penumetcha M, Rupp JC, Garvey WT.

Am J Clin Nutr. 2010. Orange juice neutralizes the proinflammatory effect of a high-fat, high-carbohydrate meal and prevents endotoxin increase and Toll-like receptor expression. Ghanim H, et al.

The Inflammatory Syndrome: The Role of Adipose Tissue Cytokines in Metabolic Disorders Linked to Obesity. Brent E. Wisse.

Crit Care Med. 2009 Oct;37(10):2727-32. Pretreatment with stress cortisol enhances the human systemic inflammatory response to bacterial endotoxin. Yeager MP, Rassias AJ, Pioli PA, Beach ML, Wardwell K, Collins JE, Lee HK, Guyre PM.

J Endocrinol. 2013 Apr 15;217(2):175-84. Acute Psychological Stress Results in the Rapid Development of Insulin Resistance. Li L, Li X, Zhou W, Messina JL.

Diabetes Care. 2007 Oct;30(10):2529-35. Epub 2007 Jun 22. Association of Oxidative Stress, Insulin Resistance, and Diabetes Risk Phenotypes: the Framingham Offspring Study. Meigs JB, Larson MG, Fox CS, Keaney JF Jr, Vasan RS, Benjamin EJ.

Obesity (Silver Spring). 2015 Apr;23(4):720-4. Early Skeletal Muscle Adaptations to Short-Term High-Fat Diet in Humans Prior to Changes in Insulin Sensitivity. Anderson AS, Haynie KR, McMillan RP, Osterberg KL, Boutagy NE, Frisard MI, Davy BM, Davy KP, Hulver MW.

PLoS One. 2013 May 21;8(5):e63983. Effect of Lipopolysaccharide on Inflammation and Insulin Action in Human Muscle. Liang H, Hussey SE, Sanchez-Avila A, Tantiwong P, Musi N.

Front Endocrinol (Lausanne). 2014 Jul 21;5:118. Estradiol Binds to Insulin and Insulin Receptor Decreasing Insulin Binding in vitro. Root-Bernstein R, Podufaly A, Dillon PF.

Mediators Inflamm. 2016;2016:6456018. Lactate, a Neglected Factor for Diabetes and Cancer Interaction. Wu Y, Dong Y, Atefi M, Liu Y, Elshimali Y, Vadgama JV.

Int J Epidemiol. 2010 Dec;39(6):1647-55. Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Crawford SO, Hoogeveen RC, Brancati FL, Astor BC, Ballantyne CM, Schmidt MI, Young JH.

Endocr Res. 2002 Nov;28(4):325-30. Oxidized products of linoleic acid stimulate adrenal steroidogenesis. Goodfriend TL, Ball DL, Raff H, Bruder ED, Gardner HW, Spiteller G.

Diabetes Care. 2015 Oct;38(10):1820-6. Fasting until noon triggers increased postprandial hyperglycemia and impaired insulin response after lunch and dinner in individuals with type 2 diabetes: a randomized clinical trial. Jakubowicz D, Wainstein J, Ahren B, Landau Z, Bar-Dayan Y, Froy O.

Blood. 2013 Feb 7;121(6):1008-15. Platelet serotonin promotes the recruitment of neutrophils to sites of acute inflammation in mice. Duerschmied D, Suidan GL, Demers M, Herr N, Carbo C, Brill A, Cifuni SM, Mauler M, Cicko S, Bader M, Idzko M, Bode C, Wagner DD.

J Steroid Biochem Mol Biol. 1992 Sep;42(8):855-61. Polyunsaturated fatty acids decrease the apparent affinity of vitamin D metabolites for human vitamin D-binding protein. Bouillon R, Xiang DZ, Convents R, Van Baelen H.

Obes Facts. 2016;9(1):1-11. Gut Microbiota and Metabolic Endotoxemia in Young Obese Mexican Subjects. Radilla-Vázquez RB, Parra-Rojas I, Martínez-Hernández NE, Márquez-Sandoval YF, Illades-Aguiar B, Castro-Alarcón N.

Exp Ther Med. 2016 Oct;12(4):2497-2500. Association between insulin resistance and estrogen in sexual precocity of obese children. Lin S, Ji W.

Diabetes. 2008 Apr;57(4):836-40. Activation of central lactate metabolism lowers glucose production in uncontrolled diabetes and diet-induced insulin resistance. Chari M, Lam CK, Wang PY, Lam TK.

Muscles Ligaments Tendons J. 2011 Dec 29;1(2):48-50. Chronic peripheral administration of serotonin inhibits thyroid function in the rat. Sullo A, Brizzi G, Maffulli N.

Nature Cell Biology volume 10, pages1421–1430(2008). Transient receptor potential M3 channels are ionotropic steroid receptors in pancreatic β cells. Thomas F.J. Wagner, Sabine Loch, Sachar Lambert, Isabelle Straub, Stefanie Mannebach, Ilka Mathar, Martina Düfer, Annette Lis, Veit Flockerzi, Stephan E. Philipp & Johannes Oberwinkler.

Diabetes Care. 2011 Aug;34(8):1809-15. Bacterial Endotoxin Activity in Human Serum Is Associated With Dyslipidemia, Insulin Resistance, Obesity, and Chronic Inflammation. Lassenius MI, Pietiläinen KH, Kaartinen K, Pussinen PJ, Syrjänen J, Forsblom C, Pörsti I, Rissanen A, Kaprio J, Mustonen J, Groop PH, Lehto M; FinnDiane Study Group.

Diabetes Metab J. 2016 Apr;40(2):89-98. Serotonin as a New Therapeutic Target for Diabetes Mellitus and Obesity. Oh CM, Park S, Kim H.

Front Cardiovasc Med. 2017 Jul 20;4:48. The Effects of Serotonin in Immune Cells. Herr N, Bode C, Duerschmied D.

J Endocrinol Invest. 2003 Jul;26(7):655-9. Is hyperprolactinemia associated with insulin resistance in non-obese patients with polycystic ovary syndrome? Bahceci M, Tuzcu A, Bahceci S, Tuzcu S.

Life Sci. 1993;53(20):1545-55. Serotonin-mediated acute insulin resistance in the perfused rat hindlimb but not in incubated muscle: a role for the vascular system. Rattigan S, Dora KA, Colquhoun EQ, Clark MG.

Horm Metab Res. 2016 Dec;48(12):787-794. Thyroid Function in Human Obesity: Underlying Mechanisms. Fontenelle LC, Feitosa MM, Severo JS, Freitas TE, Morais JB, Torres-Leal FL, Henriques GS, do Nascimento Marreiro D.

Circ Shock. 1979;6(4):333-42. Resistance of essential fatty acid-deficient rats to endotoxic shock. Cook JA, Wise WC, Callihan CS.

Nutr Hosp. 2012 Mar-Apr;27(2):382-90. The influence of endotoxemia on the molecular mechanisms of insulin resistance. Boroni Moreira AP, de Cássia Gonçalves Alfenas R.

Curr Opin Endocrinol Diabetes Obes. 2011 Apr;18(2):139-43. Obesity, Insulin Resistance and Free Fatty Acids. Boden G.

Diabetes. 2005 May;54(5):1340-8. A role for iNOS in fasting hyperglycemia and impaired insulin signaling in the liver of obese diabetic mice. Fujimoto M, Shimizu N, Kunii K, Martyn JA, Ueki K, Kaneki M.

J Nutr Sci Vitaminol (Tokyo). 1995 Apr;41(2):207-16. Polyunsaturated fatty acid-mediated suppression of insulin-dependent gene expression of lipogenic enzymes in rat liver. Iritani N, Fukuda H.

Hepatology International, June 2013, Volume 7, Issue 2, pp 516–523, Oxidative stress is closely associated with insulin resistance in genotypes 1 and 3 chronic hepatitis C. Said M. Hashemi, David van der Poorten, Francisco Barrera, Priyanka Bandara, Ora Lux, James Kench, Jacob George.

Metabolism. 2017 Mar;68:133-144. Metabolic endotoxemia and diabetes mellitus: A systematic review. Gomes JMG, Costa JA, Alfenas RCG.

J Clin Invest. 2001 Aug;108(3):437-46. Prevention of fat-induced insulin resistance by salicylate. Kim JK, Kim YJ, Fillmore JJ, Chen Y, Moore I, Lee J, Yuan M, Li ZW, Karin M, Perret P, Shoelson SE, Shulman GI.

Diabetes. 2005 Dec;54(12):3458-65. Free Fatty Acids Produce Insulin Resistance and Activate the Proinflammatory Nuclear Factor-κB Pathway in Rat Liver. Boden G, She P, Mozzoli M, Cheung P, Gumireddy K, Reddy P, Xiang X, Luo Z, Ruderman N.

Psychoneuroendocrinology. 2016 Sep;71:102-9. Executive functioning and diabetes: The role of anxious arousal and inflammation. Murdock KW, LeRoy AS, Lacourt TE, Duke DC, Heijnen CJ, Fagundes CP.

Mol Cell Neurosci. 2007 Nov;36(3):305-12.  Antidepressants induce cellular insulin resistance by activation of IRS-1 kinases. Levkovitz Y, Ben-Shushan G, Hershkovitz A, Isaac R, Gil-Ad I, Shvartsman D, Ronen D, Weizman A, Zick Y.

J Epidemiol. 2016 Jul 5;26(7):355-60. Investigation of the Relationship Between Chronic Stress and Insulin Resistance in a Chinese Population. Yan YX, Xiao HB, Wang SS, Zhao J, He Y, Wang W, Dong J.

Diabetes. 2013 Feb;62(2):346-8.  Aging and Insulin Resistance: Just Say iNOS. Evans JL, Goldfine ID.

Turk J Gastroenterol. 2016 Jul;27(4):361-6. Role of oxidative stress and insulin resistance in disease severity of non-alcoholic fatty liver disease. Köroğlu E, Canbakan B, Atay K, Hatemi İ, Tuncer M, Dobrucalı A, Sonsuz A, Gültepe I, Şentürk H.

J Clin Invest. 2002 May;109(10):1321-6. Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes. Hundal RS, Petersen KF, Mayerson AB, Randhawa PS, Inzucchi S, Shoelson SE, Shulman GI.

J Cell Biochem. 1999 Jun 15;73(4):563-72. Direct effects of prolactin on corticosterone release by zona fasciculata-reticularis cells from male rats. Chang LL, Lo MJ, Kan SF, Huang WJ, Chen JJ, Kau MM, Wang JL, Lin H, Tsai SC, Chiao YC, Yeh JY, Wun WS, Wang PS.

J Exp Med. 2005 Aug 15;202(4):517-27. 11β-HSD1 inhibition ameliorates metabolic syndrome and prevents progression of atherosclerosis in mice. Hermanowski-Vosatka A, Balkovec JM, Cheng K, Chen HY, Hernandez M, Koo GC, Le Grand CB, Li Z, Metzger JM, Mundt SS, Noonan H, Nunes CN, Olson SH, Pikounis B, Ren N, Robertson N, Schaeffer JM, Shah K, Springer MS, Strack AM, Strowski M, Wu K, Wu T, Xiao J, Zhang BB, Wright SD, Thieringer R.

Sci Rep. 2017 Aug 23;7(1):9265. iNOS promotes hypothalamic insulin resistance associated with deregulation of energy balance and obesity in rodents. Katashima CK, Silva VRR, Lenhare L, Marin RM, Carvalheira JBC.

PLoS One. 2017 Jul 6;12(7):e0180745. Regulation of gut luminal serotonin by commensal microbiota in mice. Hata T, Asano Y, Yoshihara K, Kimura-Todani T, Miyata N, Zhang XT, Takakura S, Aiba Y, Koga Y, Sudo N.

PLoS One. 2012;7(6):e38734. Activation of Pregnane X Receptor by Pregnenolone 16 α-carbonitrile Prevents High-Fat Diet-Induced Obesity in AKR/J Mice. Ma Y, Liu D.

Diabetologia. 2008 Jan;51(1):139-46. Oral taurine but not N-acetylcysteine ameliorates NEFA-induced impairment in insulin sensitivity and beta cell function in obese and overweight, non-diabetic men. Xiao C, Giacca A, Lewis GF.

Open Cardiovasc Med J. 2011;5:153-63. Regulation of Inducible Nitric Oxide Synthase (iNOS) and its Potential Role in Insulin Resistance, Diabetes and Heart Failure. Soskić SS, Dobutović BD, Sudar EM, Obradović MM, Nikolić DM, Djordjevic JD, Radak DJ, Mikhailidis DP, Isenović ER.

Diabetes Metab Res Rev. 1999 Nov-Dec;15(6):427-41. Neuroendocrine perturbations as a cause of insulin resistance. Björntorp P.

Am J Physiol Regul Integr Comp Physiol. 2003 Jun;284(6):R1631-5. An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells. Bruder ED, Ball DL, Goodfriend TL, Raff H.

PLoS Biol. 2013;11(2):e1001485. Partial Inhibition of Adipose Tissue Lipolysis Improves Glucose Metabolism and Insulin Sensitivity Without Alteration of Fat Mass. Girousse A, Tavernier G, Valle C, Moro C, Mejhert N, Dinel AL, Houssier M, Roussel B, Besse-Patin A, Combes M, Mir L, Monbrun L, Bézaire V, Prunet-Marcassus B, Waget A, Vila I, Caspar-Bauguil S, Louche K, Marques MA, Mairal A, Renoud ML, Galitzky J, Holm C, Mouisel E, Thalamas C, Viguerie N, Sulpice T, Burcelin R, Arner P, Langin D.

Mol Metab. 2016 Dec 19;6(2):206-218. Blocking iNOS and endoplasmic reticulum stress synergistically improves insulin resistance in mice. Zanotto TM, Quaresma PGF, Guadagnini D, Weissmann L, Santos AC, Vecina JF, Calisto K, Santos A, Prada PO, Saad MJA.

Br J Nutr. 2012 Jan;107(1):86-95. Chronic caffeine intake decreases circulating catecholamines and prevents diet-induced insulin resistance and hypertension in rats. Conde SV, Nunes da Silva T, Gonzalez C, Mota Carmo M, Monteiro EC, Guarino MP.

Med Hypotheses. 1999 May;52(5):401-6. High-dose biotin, an inducer of glucokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes. McCarty MF.

Biomed Pharmacother. 2017 Oct;94:380-385. Minocycline Attenuates Severe Hyperglycemia in Patient with Lipodystrophy. Yang C, Gao J, Wu B, Yan N, Li H, Ren Y, Kan Y, Liang J, Jiao Y, Yu Y.

PLoS One. 2017 Apr 6;12(4):e0175204. Association between serum prolactin levels and insulin resistance in non-diabetic men. Daimon M, Kamba A, Murakami H, Mizushiri S, Osonoi S, Yamaichi M, Matsuki K, Sato E, Tanabe J, Takayasu S, Matsuhashi Y, Yanagimachi M, Terui K, Kageyama K, Tokuda I, Takahashi I, Nakaji S.

Cell. 2015 Apr 9;161(2):264-76. Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis. Yano JM, Yu K, Donaldson GP, Shastri GG, Ann P, Ma L, Nagler CR, Ismagilov RF, Mazmanian SK, Hsiao EY.

Cardiovasc Diabetol. 2015 May 20;14:56. Tissue inflammation and nitric oxide-mediated alterations in cardiovascular function are major determinants of endotoxin-induced insulin resistance. House LM 2nd, Morris RT, Barnes TM, Lantier L, Cyphert TJ, McGuinness OP, Otero YF.

Endocr Res. 2002 Nov;28(4):325-30. Oxidized products of linoleic acid stimulate adrenal steroidogenesis. Goodfriend TL, Ball DL, Raff H, Bruder ED, Gardner HW, Spiteller G.

Biogerontology. 2012 Apr;13(2):93-103. High-fat diet intake accelerates aging, increases expression of Hsd11b1, and promotes lipid accumulation in liver of SAMP10 mouse. Honma T, Shinohara N, Ito J, Kijima R, Sugawara S, Arai T, Tsuduki T, Ikeda I.

Jpn J Vet Res. 2012 Feb;60(1):5-13. Changes in blood glucose and insulin responses to intravenous glucose tolerance tests and blood biochemical values in adult female Japanese black bears (Ursus thibetanus japonicus). Kamine A, Shimozuru M, Shibata H, Tsubota T.

Life Sci. 1988;42(13):1323-30. Biotin supplementation improves glucose and insulin tolerances in genetically diabetic KK mice. Reddi A, DeAngelis B, Frank O, Lasker N, Baker H.

Diabetes Care. 2002 Mar;25(3):500-4. The Effect of Estrogen Use on Levels of Glucose and Insulin and the Risk of Type 2 Diabetes in American Indian Postmenopausal Women. Zhang Y, Howard BV, Cowan LD, Yeh J, Schaefer CF, Wild RA, Wang W, Lee ET.

Can J Diabetes. 2015 Feb;39(1):36-43. Macrophages Inhibit Insulin Signalling in Adipocytes: Role of Inducible Nitric Oxide Synthase and Nitric Oxide. Fite A, Abou-Samra AB, Seyoum B.

Alzheimers Dement. 2014 Feb;10(1 Suppl):S26-32. How does brain insulin resistance develop in Alzheimer’s disease? De Felice FG, Lourenco MV, Ferreira ST.

Diabetes. 2005 Jul;54(7):1926-33. A high-fat diet coordinately downregulates genes required for mitochondrial oxidative phosphorylation in skeletal muscle. Sparks LM, Xie H, Koza RA, Mynatt R, Hulver MW, Bray GA, Smith SR.

Diab Vasc Dis Res. 2008 Jun;5(2):76-81. Mammalian hibernation: a naturally reversible model for insulin resistance in man? Martin SL.

Biochem Soc Trans. 2005 Nov;33(Pt 5):1045-8. Review. Adipose tissue function in the insulin-resistance syndrome. Karpe F, Tan GD.

J Clin Invest. 2006 Jul;116(7):1793-801. Review. Inflammation and insulin resistance. Shoelson SE, Lee J, Goldfine AB.

J Clin Invest. 1996 Jun 15;97(12):2859-65. Mechanism of free fatty acid-induced insulin resistance in humans. Roden M, Price TB, Perseghin G, Petersen KF, Rothman DL, Cline GW, Shulman GI.

Behav Neurosci. 2013 Jun;127(3):400-14. Effects of Aromatase Inhibition and Androgen Activity on Serotonin and Behavior in Male Macaques. Bethea CL, Reddy AP, Robertson N, Coleman K.

Scientific Reports volume 6, Article number: 19495 (2016). Alterations of the volatile metabolome in mouse models of Alzheimer’s disease. Bruce A. Kimball, Donald A. Wilson & Daniel W. Wesson.

Neth J Med. 2013 May;71(4):174-87. Review. Obesity-associated low-grade inflammation in type 2 diabetes mellitus: causes and consequences. van Greevenbroek MM, Schalkwijk CG, Stehouwer CD.


Image: FoodsMatter: “Probiotics – the ‘friendly’ bacteria:” John Scott

You may also like...

4 Responses

  1. Avatar ananta says:

    I may have potentially developed Sibo and low thyroid function due to 20 years of vegan food life- style and was going to try 30 -day high -fat carnivore meat and eggs only elimination diet prompted by Paleomedicina in hungary where they had outstanding results on 1000s of autoimmune disease and diabetes patients. Then while I was researching carnivore, keto diet I also stumble upon Ray peat’s blogs like yours. I am confused.. what do you think of the paleomedicina’s approach, please?

  2. DanM@cowseatgrass DanM@cowseatgrass says:

    I don’t know it specifically, but these types of diets can be beneficial because of initial endotoxin reduction due to the removal of many difficult to digest ingredients. Long term there are issues because of increased stress and inflammation, and reduced thyroid metabolism etc. due to the removal of sugar from the diet, and because of high fat intake and some other issues. How beneficial it is, is also influenced by how success or health improvement is being determined.

  3. Avatar Nitin says:

    Good morning, Namaste. I am from India and reading your articles since last more than six months. I was immensely helped with the (so called contradictory!) information, particularly with respect to the sugar consumption, and I am thankful to you. My story may be beneficial to someone.

    I was healthy (male, in my 40s), vegetarian (eggs allowed, but no meat and fish), fond of exercise, trekking etc and for no reason started intermittent fasting and raw food regime. With in three years, I lost from 65 kg to 49 kg and then one day the body collapsed. By that time I had lost my ability to digest food and developed high BP, high TSH, (FT3, FT4 within range but lowish), food intolerances etc etc. I was not able to walk even few steps and had constant nausea, dizziness. Doctors diagnosed it as acidity with IBS/SIBO. Since I knew why I have collapsed, I refused all allopathic medicines and went for wholistic system like the one of Ayurveda. Unfortunately, visiting Ayurvedic practitioners worsened my situation! I then started studying general principles of Ayurveda myself and surprisingly, what I found was in sync with what you mention in your articles.

    The ancient system classifies three types of Mind – Body constitutions, viz Kapha, Pitta and Vata. (more on this can be easily found out in numerous reputed websites and blogs). Every person is a combination of all three with one of the humor dominating. As per Ayurveda, the later two are prone to stress, anger, anxiety etc etc. As repeatedly highlighted in your articles, our present day life style has given rise to increased stress, and as a result, the Pitta and Vata humors might be getting vitiated resulting in all sorts of diseases and complications. Ayurveda recommends dietary guidelines to pacify vitiated Pitta and Vata humors. First of all, both types of persons are not advised to fast at all. For Pitta the recommendation is to consume more of sweet, bitter and astringent foods and for Vata it is sweet, sour and salty foods. Sweet and milk is common for both. As a matter of fact, the raw sugar (called as misry ) is praised in Ayurveda as being cooling, strengthening and tonic which pacifies both Vata and Pitta humor. People in India used to eat lots of sweets made up of milk and sugar. Our elders used to say, ‘God showers good things on him who consumes lots of sweets’! We worship deities in the temple and the food offerings to them is invariably some type of sweet.

    Unfortunately, with the onslaught of the so called mainstream medical recommendations, more and more people are refraining from sweet consumption. Even the Ayurvedic practitioners are falling pray to these, and asking people to cut the sugar consumption. Almost all the Ayurvedic doctors I visited asked me to restrict sugar. It needs to be noted here that most of the Ayurvedic herbs have blood glucose lowering effect and not surprisingly, I felt worse after taking them. Sometimes after consuming a heavy dose, I used to collapse and invariably felt ok after consuming some sugar.

    It was after suffering for more than 3-4 years that I came across your blog. It gave me some confidence that sugar is something I need. Before getting in to the fad of raw food and fasting, I was a foodie and used to eat everything including milk based sweets. And since Ayurveda too is not against the sugar (for persons with Pitta and Vata constitution), I decided to give it a try. I started consuming sugar in three different ways. In sweet preparations like rice or wheat pudding, in low fat milk and in raw form, 1 tsp, after breakfast, lunch and dinner. And what a wonder, I started feeling the difference within 3-4 days! My energy levels improved, the collapsing episodes almost vanished, TSH came down to 3 from 10, and most importantly most of my food intolerances went away! I also discontinued all the herbal medicines prescribed by doctors and started taking one particular herb which Ayurveda highly recommends for it’s cooling, strengthening and calming effect. It is now almost 4 months and I am much much better. For the first time in last 4 years, I again went to Himalayas and did long and ardours treks to my satisfaction. I feel like winning my life back. I cant say I am fully recovered. I still sometimes feel flared up after eating particular food and have occasional nausea and dizziness. After all, it may not be possible to recover fully at this age if irreversible damage is inflicted due to the 3 years of raw food consumption coupled with fasting and heavy exercising. But one thing is certain, bringing back the sugar has qualitatively changed my health.

    I am also silently observing many persons in and around me, who after cutting their sugar intake are experiencing health issues. But the grip of main stream recommendation is firm. People have surrendered all logics to doctors.

    So again, thanks for the articles which was a game changer for me.

    PS : Long back in one of the blogs (I don’t remember which one), a naturopath in India mentioned about treating IBS in one youth by simply feeding him one tsp of table sugar every hour for three days. As per the blog, the fellow was cured of all the symptoms within that period!

  4. DanM@cowseatgrass DanM@cowseatgrass says:

    Great to hear, thank you and thank God.

Leave a Reply

Your email address will not be published. Required fields are marked *

Please "like" us:Already liked? You can close this