[ Diabetes Solutions ]

Nutrition & Metabolism

Psoriasis is a systemic, immune-mediated disorder, characterized by inflammatory skin and joint manifestations. Atherosclerosis is intrinsically an inflammatory disease. This epidemic is likely to drive previously unforeseen rates of vascular target organ complications. AAT is an acute phase protein and its level increases during inflammation. Assessments were performed prior to and at 3 and 6 months after treatment and included probing depth (PD), clinical attachment level (CAL), detection of Porphyromonas gingivalis in subgingival plaque and determination of serum glucose and glycated hemoglobin (HbA1c). When you don’t have enough insulin, or your body cannot use insulin properly, the amount of glucose in the blood becomes too high. Because the major contributing factor for insulin resistance is currently considered to be the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), and because periodontal surgery may cause transient bacteremia which may up-regulate the serum TNF-alpha level, which in turn suppresses insulin action, patients should be strictly treated non-surgically and their serum TNF-alpha levels should be periodically monitored.

This study tested the hypothesis that risks of CHD, stroke and T2DM are consistently elevated across a range of inflammatory diseases affecting either single systems or involving multiple systems. In contrast, the retinas from diabetic ICAM-1 and CD18 competent mice exhibit marked increases in leucocyte density, blood-retinal barrier breakdown, and endothelial cell injury and death. Comment in: Gastroenterology 2009;136:1164-1167. The current Western diet can disturb the resolution response in various ways (Figure 6 ). In the Ancestral human diet, foodstuffs with an increased risk of inflammation were virtually unknown, while nutrients able to activate the IIS are now abundant in our diet [ 38 , 120 ]. Your doctor will likely have you take antibiotics to treat PID. And dairy foods may help ease inflammation in patients with a combination of risk factors.


If our genes are exposed to their ‘original’ environment by intake of an ancestral human diet, their function can recover rapidly. These include the Toll Like Receptors (TLRs) and the receptor for advanced glycation end products (RAGE). Similar results have been found in a study with aboriginals suffering from Diabetes II, who showed normalized blood markers after returning to their traditional lifestyle for seven weeks [ 122 ]. Still, PID remains a significant women’s health problem. McGowan et al [123] show the impact of childhood abuse on the epigenetic pattern of different genes including the gene for GR in the hippocampus. Many studies have examined the variability of candidate genes in diverse pathogenic pathways for this complication, including the renin-angiotensin, nitric oxide, and bradykinin systems. 1).

An altered sensitivity to cortisol has been linked to diseases such as rheumatoid arthritis (RA) [124], post-traumatic stress syndrome [125], chronic fatigue syndrome [126], inflammatory diseases and AID in general [127]. The key priority in the treatment of people with chronic inflammation is to induce the Eicosanoid Switch to the anti-inflammatory resolution phase. This can be partially explained by lifestyle choices and diet. Gerszten RE, Garcia-Zepeda EA, Lim YC, Yoshida M, Ding HA, Gimbrone MA, Jr., et al. Figure 7 Chronic over-activation of the systemic stress system as a result of external stressors plays a central role in the development of chronic inflammatory diseases. Current intervention with anti-inflammatory medication suppresses Resoleomics and the IIS and so enhance the over-activation of the systemic stress system. Current anti-inflammatory medication used in RA treatment is aimed at the suppression of the IIS and its inflammatory response and thus hinders Resoleomics.

In addition, these medication interventions do not solve underlying catecholamine, cortisol and insulin resistance, and consequently making it impossible to achieve full recovery of the chronic inflammation. This suggests that chronic use of anti-inflammatory medication in fact impedes the body from making a full recovery. Furthermore, the ongoing low-grade inflammation will continuously trigger the activity of the systemic stress system [28]. Health care should focus on early detection of silent, ongoing and low-grade inflammation in order to avoid the development of many chronic diseases. Plants are by far your best inflammation-fighting bet. We have made an effort to demonstrate that the science of Resoleomics can help to find new ways to treat people suffering from diseases based on chronic inflammation. Since over-activated central stress axes directly delay Resoleomics, and thereby delay the resolution of inflammation, treatment should focus on restoring the central stress system to its default, healthy homeostasis.

Dietary changes, psycho-emotional stress release and physical activity should always be included in treatment of all chronic inflammatory diseases.

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[ Diabetes Solutions ]

Nutrition & Metabolism

Acetyl-L-carnitine reduces the latencies of electroretinogram oscillatory potentials in healthy humans. It is  considered an alternative treatment for the disease and, when it is used, it is used in the management of diabetic neuropathy, which is diabetic nerve pain of the feet, hands, and legs that causes numbness and/or burning pain from glucose affecting the nerves. 14CO2 release from [1-14C]pyruvate (an index of PDH activity), [2-14C]pyruvate and [6-14C]glucose (an index of acetyl-CoA flux through the Krebs cycle), [U-14C]glucose (an index of both PDH and acetyl-CoA flux through the Krebs cycle), and [1-14C]palmitate oxidation were studied in cardiac myocystes isolated from normal and streptozotocin-injected rats. In addition, ALC is known to produce a strong antinociceptive effect when given after neuropathic pain has been established. ALC also affected the formation of antibodies to AGEs. It is also used for Down syndrome, poor circulation in the brain, cataracts, nerve pain due to diabetes, nerve pain due to drugs used in the treatment of AIDS, and facial paralysis. However, certain medical conditions and medications may limit the body’s ability to produce enough, making supervised supplementation necessary.

We conclude that in animals hyperglycemic long enough to slow NCV, sorbinil and/or ALC treatment reduces the functional, structural, and biochemical changes associated with hyperglycemia that occur in the myelin sheath. Results: Treatment periods differ (range: 120–16 months) because children began treatment at different times. Possibly Effective for… Our failure to note any significant effect of ALCA in regards to this panel provides convincing evidence that no treatment effect related to postprandial oxidative stress is noted with supplementation, at least at the dosage (3 g·day-1) and for the duration (8 weeks) provided. This, despite the fact that our chosen treatment included L-arginine, a known precursor to nitric oxide biosynthesis [34], as one component of the supplement. Liu noted: “Lipoic acid and acetyl-L-carnitine have become very hot after our reports on the complementary effects on improving memory and ambulatory activity in old rats,” relating to studies published in the Proceedings of the National Academy of Science in 2002 (Vol. Our data related to nitrate/nitrite provide partial support for the findings of improved FMD with carnitine intake [29], as nitric oxide is known to facilitate vasodilatation by acting on vascular smooth muscle cells [30].

In the months following a severe heart attack, the left ventricle of the heart often enlarges, and the pumping action of the heart becomes less efficient. Hierbij speelt acetyl-L-carnitine een rol. [29] may have. This is particularly true for the extremely small, but statistically significant findings of Volek et al. [29], who noted an increase in postprandial (1.5 hour) FMD from 6.6% to 7.7% with carnitine treatment as compared to a decrease in FMD from 6.6% to 5.8% with placebo. While these findings were noted as statistically significant, their clinical relevance must be questioned, especially considering the somewhat subjective nature of this brachial artery imaging assessment. Moreover, no other differences were noted between carnitine and placebo at the 3.0 and 4.5 hour postprandial measurement times.

Some mild side effects may be observed such as headaches, stomach discomfort, nausea, and diarrhea. They claimed that LC deficiency was not the major cause of liver steatosis. This is particularly true considering that no other measures in this study by Volek and colleagues [29] were noted to be significantly effected by carnitine (e.g., triglycerides, malondialdehyde, insulin, interleukin-6, tumor necrosis factor-alpha). Researchers have used Acetyl L-Carnitine to help reverse peripheral nerve damage. Acetyl-L-carnitine (ALC) has been shown to facilitate the repair of transacted sciatic nerves. We have recently reported in two studies using human subjects that oral supplementation with carnitine (glycine propionyl L-carnitine) increased nitrate/nitrate at rest [32] and in response to static exercise [33]. Lofreddo and coworkers [31] have also demonstrated that intravenous injection of propionyl L-carnitine increases nitrate/nitrate in patients with peripheral arterial disease.

Second, the antioxidant effects of carnitine can provide protection against nitric oxide destruction via superoxide production [57]. L-carnitine at a dose of 3 grams daily was used by 16 people with HIV who were also taking anti-HIV drugs. Hence, carnitine may lead to both the production of nitric oxide, as well as the maintenance of existing nitric oxide. Our hypothesis for attenuation in oxidative stress biomarkers with ALCA treatment was based on a sound body of literature demonstrating antioxidant benefits of carnitine in both humans [32, 59, 60] and animals [27, 61, 62]. Our failure to note significant antioxidant effects related to our chosen biomarkers could be explained in at least two manners. First, it is possible that the dosage of ALCA used in the present study, in conjunction with the relatively large nutrient load, was not adequate to provide protection against the massive oxidative insult incurred by the test meal. Most previous studies have simply measured oxidative stress biomarkers in a rested, fasted state following carnitine administration.

Our use of the test meal may have overwhelmed the antioxidant ability of the ALCA, leading to our null results. This is particularly true considering that our test meal, although not of uncommon size and composition for meals consumed by many overweight/obese individuals, was relatively large compared to some previous studies [63–65]. This may have lead to increased radical production, possibly minimizing any positive effects of the ALCA treatment. Second, our sample consisted of pre-diabetics, thus deficiencies in postprandial glucose and lipid metabolism likely occurred in response to the test meal. Surprisingly, however, we noted only a minimal blood glucose response to feeding. This is likely due to both the timing of our measurements (i.e., first measurement occurring one hour post feeding), as well as the inclusion of a high amount of dietary fat to the test meal. Almost identical findings have been reported recently by Blendea and colleagues [66].

In addition to being pre-diabetic, our subjects were overweight or obese. We have recently noted that obese individuals experience an exaggerated lipemic and oxidative stress response to high fat, high carbohydrate feeding, as compared to normal weight subjects [45]. This increase in blood triglyceride following feeding is directly linked to superoxide production [67, 68], likely mediated by hypertriglyceridemic-induced neutrophilia [69]. Circulating triglycerides may also result in accelerated superoxide production from the abundance of substrate processing and subsequent production of reducing molecules (e.g., NADH, FADH2) generated with our large meal [70]. Obese individuals also have lower plasma antioxidants and higher tissue lipid levels which can lead to an increased susceptibility to oxidative stress [71]. Hence, our sample of pre-diabetics may have experienced too great an increase in radical production following the meal, further hampering the ability of the ALCA to provide measurable antioxidant effects. Future work may consider the use of 1) a higher dosage of ALCA, 2) smaller test meals, and 3) the use of metabolically normal test subjects in order to further determine the potential antioxidant benefits of ALCA in relation to postprandial oxidative stress and associated biomarkers.

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[ Herbal Remedies ]

Nutrition & Metabolism

Inflammation is thought to be one of the major factors in all kinds of diseases, and turmeric contains loads of curcumin, a powerful anti-inflammatory substance. Otherwise, you’re a prime candidate for type 2 diabetes and all the complications that come with it, including an elevated risk of heart disease; nerve, kidney, and eye damage; Alzheimer’s disease; and amputations. The curcumin was able to trigger a significant reversal of the condition. It’s easy to grow in all sorts of climates. But it’s not just those who already have diabetes who benefit from using turmeric. Curcumin, the active ingredient in Turmeric, has been in the news lately because of the innumerable benefits of consuming it. The high morbidity and mortality for diabetic cardiomyopathy warrant aggressive clinical management involving lifestyle modification, control of glucose and lipid abnormalities, and treatment of hypertension and coronary artery diseases, if present.

Curcumin because of the various actions as detailed in the figure is able to effectively prevent development of microangiopathy and hence development of these complications. The randomised control trial will test both compounds, with the recruitment group being segregated into four. In this study, people with high risk factors for developing diabetes were assigned either to a placebo or to the supplement curcumin. GSH, an intracellular antioxidant, is important in antioxidant defense, nutrient metabolism, and regulation of cellular events, including gene expression, apoptosis and cytokine production [26]. Therefore, NC‑induced DN progression may predominantly operate by increasing oxidative stress, reducing the levels of antioxidants, suppressing EPO levels, and causing perturbations to gap junction and podocyte structure. Here, we provide data demonstrating that curcumin administration has partial beneficial effect on diabetes-induced decrease in retinal GSH; the GSH levels in curcumin-treated diabetic rats remained significantly lower than those in the normal control rats, but were significantly higher than diabetic rats. Overall Health: The antioxidants and phytonutrients in turmeric improves the general health.


Turmeric is available in the form of a rhizome, powder, capsule, tincture and oil. Or, there could be compartmentalization of GSH in the retina, and levels could possibly be normalized in the cells associated with the development of diabetic retinopathy. The therapies that inhibit diabetes-induced nitrotyrosine accumulation in the retina are shown to inhibit diabetic retinopathy [22, 29, 30]. Here we demonstrate that curcumin can prevent diabetes-induced increase in nitrotyrosine levels in the retina. In support, curcumin has been reported to inhibit diabetes-induced increased nitrotyrosine immunostaining in the heart [25], and also is postulated to exert its neuroprotective effects and prevent alcohol-induced liver damage via regulating peroxynitrite levels [31, 32]. Diabetic retinopathy shares similarities with low level chronic inflammatory disease, and subclinical inflammation is considered to play a role in the vascular lesions characteristic of diabetic retinopathy [33]. They found that nano-emulsified curcumin halted the recruitment of immune cells called macrophages that “eat” invading pathogens but also contribute to inflammation by secreting pro-inflammatory chemicals.

It describes the ability of a blood vessel in the arm to dilate – “open up” – after blood flow is stopped with a blood pressure cuff then released. ROS are considered as strong stimuli for the release of cytokines, and IL-1β itself can trigger signaling cascades resulting in excessive ROS [14]. Our data demonstrate that curcumin, a compound with both anti-inflammatory and antioxidant properties, prevents diabetes-induced increase in IL-1β. This suggests that curcumin could inhibit the development of diabetic retinopathy by inhibiting both, proinflammatory cytokines and oxidative stress. IL-1β induces the expression of various genes whose promoters are regulated through complex interactions with NF-k B [35]. What does this mean? We have shown that NF-k B is activated in the retina and its capillary cells in diabetes, and its activation is an early event in the development of retinopathy that is sustained when retinal capillary cell death is accelerating, and histopathology is developing [29].

In the pathogenesis of diabetic retinopathy activation of NF-k B is reported to trigger a developing pro-apoptotic program in retinal pericytes [38], and accelerated apoptosis can predict the development of retinopathy in diabetes [39]. Aleeva et al. Turmeric is commonly used as natural pigment (yellow 3) in the cosmetic and textile production but it is widely used in food industry. Diabetic retinopathy is accompanied by elevation in various angiogenic factors, and VEGF, a hypoxia-induced growth factor, is considered to play a pivotal role in the increased permeability and angiogenesis seen in diabetic retinopathy [15]. Oxidative stress is considered to regulate diabetes-induced retinal VEGF levels [40]. Our data clearly show that curcumin administration inhibits increased VEGF levels in the retina. In agreement, others have shown that curcumin can abolish IL-18 induced increase in VEGF production [41].

The beneficial effects of curcumin observed in the present study were achieved without amelioration of the severity of hyperglycemia in diabetic rats; the blood glucose, urine volume and body weights were similar in diabetic rats and diabetes + curcumin rats. Curcumin is shown to be safely tolerated, clinical trials using up to 8000 mg curcumin per day for 3 months have shown no toxicity to curcumin [42]. Based on the food consumption, the rats in our experiment consumed about 16 mg curcumin per day (about 80 mg/kgBW), and this concentration is within the range of the concentration used for clinical trials. However, curcumin has poor oral bioavailability [43] that could limit its full potential in the retina. It’s hard to say how long it will take for you to see results. Although, due to tissue limitations, direct measurements of curcumin levels in the retina were not made, the beneficial effects of curcumin observed in our study imply that curcumin was able to cross the blood-retina barrier. This is supported by others showing that curcumin can cross the blood-brain barrier in mice, and brain curcumin levels achieved are comparable to the levels achieved in the plasma [45].

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[ Nutrition ]

Nutrition & Metabolism

Obesity is a major risk factor for the development of type 2 diabetes, and both conditions are now recognized to possess significant inflammatory components underlying their pathophysiologies. Out of all the supplements I’ve ever tried, I don’t think I’ve ever had one that actually made a radical difference in the way I feel. Research shows curcumin is powerful and versatile when it comes to health (and cancer, in particular). That’s a lot of promise in a capsule! We also examine whether the up regulation of HO-1 accompanied by increased HO activity mediates these antidiabetic and anti oxidant actions. Phenylephrine (PE)-induced contraction was significantly (P < 0.05) increased during the early stage of diabetes, whereas it was significantly (P < 0.05) reduced at the medium and late stage of diabetes. Curcumin was dissolved in dimethyl sulfoxide (DMSO) and used as inhibitor of alpha amylase. The curcumin and identical placebo capsules were manufactured by the Government Pharmaceutical Organization of Thailand. Ghosh et al.[28] showed that curcumin treatment improved kidney function in animals with chronic renal failure by antagonizing the effect of TNF-α elicited NF-κB activation and macrophage infiltration, indicating that the anti-inflammatory property of curcumin may be responsible for alleviating chronic renal failure in nephrectomized animals. There’s plenty of solid scientific data surrounding this ingredient’s potential. Chiu et al. Endothelial dysfunction is the ability of endothelium to control blood clotting, blood pressure and various other factors. Source: Malaysian Diabetes Association (PDM), 2012. However, it is still unknown whether anti-inflammatory mechanism of curcumin through the inhibition of macrophage infiltration, might offer the renal protective effect in type I. In addition to exploring novel methods of curcumin administration to increase its absorption, they are also interested in identifying novel anti-inflammatory processes invoked by curcumin and in adapting those processes in the development of more potent curcumin analogues. Schmid et al. have reported that upregulation of NF-κB targets, a master transcriptional gene play a role in inflammatory response in the kidney of the patients with progressive DN [38]. In one study, participants who took curcumin had a significantly lower relapse rate compared to those who consumed a placebo. After activation by a number of physiological and nonphysiological stimuli, such as IL-1β, TNF-α, or lipopolysaccharide, IκB dissociates from NF-κB within minutes and undergoes ubiquitination and degradation. Once NF-κB is released from the inhibitory unit IκB, the NF-κB is then translocated into the nucleus. Upon its nuclear translocation, NF-κB undergoes phosphorylation on serine 276 in its p65 subunit and associates with surrounding chromatin components.

It subsequently binds with DNA and promotes the transcription of proinflammatory cytokines, such as TNF-α and IL-1β. Previous study has reported that phosphorylation on serine 276 is essential for NF-κB p65-dependent cellular responses [39]. Therefore, measurement of the phosphorylated p65 subunit of NF-κB is an effective tool for determining NF-κB activation [12, 40]. Our results showed that activation of NF-κB and degradation of IκBα, as well as proinflammatory cytokines expression, TNF-α and IL-1β were increased in diabetic rats compared with the levels in control rats (Figures. 3 and 4). Curcumin treatment prevented all of these alterations. We believe that the curcumin’s ability to inactivate NF-κB [41] and thus inhibited the production of proinflammatory cytokines [29] is its most likely mechanisms of action.

Macrophages are known to cause early glomerular injury in STZ-induced diabetes and also to be involved in the mechanisms that cause progressive glomerular and tubular damage [5, 10, 42, 43]; in addition, ICAM-1 and MCP-1 are considered as a central molecule involved in macrophage influx in DN [9, 11, 44–46]. Park et al. have demonstrated that high glucose could upregulate ICAM-1 protein and mRNA expression in rat mesangial cells through the protein kinase C-NF-κB pathways [11, 14]. ICAM-1 is also induced by inflammatory cytokines such as TNF-α, IL-1, and interferon-γ [47]. Recent studies provided evidences that both ICAM-1 gene deficiency [10, 45] and anti-ICAM-1 monoclonal antibody [11] obviously inhibited the infiltration of monocytes/macrophages into the glomerulus and alleviated the extent of renal injury. Studies have also demonstrated that NF-κB was involved in the induction of MCP-1 in mesangial cell cultured under high glucose condition and subsequently mediated macrophage accumulation [9, 48, 49]. Consistent with these previous reports, we have also observed that ICAM-1 and MCP-1 expression were increased in rats with experimental DN (Figure 5), which was associated with marked macrophages infiltration (Figure 2), and that these increases under diabetic conditions were ameliorated by curcumin treatment.

This effect might be mediated by curcumin’s inhibition of NF-κB activation. The novel water-soluble curcumin derivative with conserved natural functional groups is [1,7-bis (5-carboxyphenylazo-4-hydroxy-3-methoxyphenyl)1,6-heptadiene-3,5-dione]. Accumulating evidence suggests that, in DN, glomerulosclerosis is associated with TGF-β1 expression [50, 51], which is related to macrophage infiltration in glomeruli [52]. TGF-β1 is assumed to mediate inflammatory response and exaggerate the progression of DN [53]. In vitro and in vivo studies have reported that macrophages stimulates mesangial cells to produce ECM proteins through TGF-β [44, 54, 55]. TGF-β can in turn induce ECM overproduction from mesangial cells in autocrine and paracrine fashions [45]. Previous study has revealed that infiltrated monocytes/macrophages release lysosomal enzymes, nitrous oxide, reactive oxygen intermediates and TGF-β, which have been reported to play an essential role in renal damage and the depletion of macrophage by irradiation decreased the gene expression of TGF-β and type IV collagen in the glomeruli of diabetic rats at 4 weeks after induction of diabetes, suggesting the pathological role of macrophages in the increased expression of ECM proteins [56, 57].

From the above results it is obvious that macrophage infiltration is an important inducer of TGF-β1. The TGF-β1 contains a sequence located -715 to -707 bp where NF-κB binds to target TGF-β1 gene expression [58]. Thus, following NF-κB activation, marked infiltration of macrophages subsequently upregulated the TGF-β1 expression which further promotes the increased ECM synthesis in diabetes. Our results show that renal TGF-β1 protein expression was significantly increased in diabetic rats. Curcumin treatment obviously decreased renal TGF-β1 expression and this improvement was achieved most probably via the inhibition of NF-κB activation. Taken together, all the above results suggest that beneficial effect of curcumin in rats with DN is at least in part through inhibition of macrophage infiltration via inhibiting NF-κB mediated inflammatory response.

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[ Nutrition ]

Nutrition & Metabolism

(This question was written before the more current “Food Plate”) Q: I have been trying to follow the Food Pyramid for quite some time. I used to eat 10 slices of bread each day but now fill up on protein and fat instead. The typical American way of eating provides 250–300 grams of carbohydrate daily. If insulin can’t keep up, and this is more likely in people with type 2 diabetes, then our blood glucose levels go too high and we can end up feeling tired and lethargic. Although plasma fasting glucose and insulin concentrations were similar with both diets, incremental glucose and insulin responses from 8 a.m. In contrast, following carbohydrate restriction lactate concentrations were initially reduced by glucose administration, this reduction taking place despite continuing lactate release from the forearm. These findings suggest that low-carbohydrate diets are at least as effective as low-fat diets at reducing weight and improving metabolic risk factors.

Plasma glucose and insulin responses to identical standard breakfast meals were studied on days 4 and 21 of each period, and these did not differ significantly between the two diets. Decreased hepatic glutathione peroxidase activity and lipid peroxidation were noted in diet-treated diabetic rats. It is significant that 44 % of the patients have had a stable weight or have reduced it further and all but one had a lower weight at 22 months than at the beginning of the study. Finally, postheparin lipoprotein lipase and hepatic lipase activities were measured at the end of each dietary period. High-protein, low-carbohydrate diets deteriorated diabetic conditions and were associated with insufficient insulin secretion in db mice. The lack of hunger and cravings with the low-carbohydrate diet may be an important reason for their present success. In the normal diabetes diet whole-grain products are recommended.

Self determination of blood glucose provides a feed-back mechanism and may be another reason that 44 % of the patients succeeded in maintaining their weight. Nut flours can be used to make some baked goods, such as muffins. This close supervision may be another reason for the patients’ initial success. Ask your doctor if you are at risk for severe hypoglycemia. Eating a lower amount of carbohydrate means less insulin is required from the pancreas, thus taking strain off the pancreas. Similarly, intentional weight loss in type 2 diabetes patients is associated with a reduced mortality of 30–40 % [17]. For the average patient each 1 kg weight loss is associated with 3–4 months prolonged survival [18] making it likely that the patients described here have achieved a survival benefit.

Given this recent additional evidence, a meta-analysis of randomized controlled trials comparing the effects of low-carbohydrate diets with those of low-fat diets on metabolic risk factors is timely and important to public health. We have examined the medical charts for both the original high-carbohydrate group and the low-carbohydrate group from 3 months after the initiation of the diet therapy – when an effect might be detected – and forward for episodes of cardiovascular disease. Three episodes of cardiovascular disease have occurred among the 5 patients that never changed diet. The 16 patients in the low-carbohydrate diet group (19 months observation time) and the 7 from the high-carbohydrate diet group that changed diet (10 months observation time) – totalling 23 patients – have been free of cardiovascular disease during the follow-up period (p < 0.03. Fischer Exact). Several recent reviews have made the case for reducing the carbohydrate load in type 2 diabetes [21–23] or metabolic syndrome [24] and the low-carbohydrate diet presented here is clearly effective in many obese people with type 2 diabetes. Because of its effectiveness it should be used with close clinical supervision in patients on insulin or oral hypoglycaemic agents. In summary, a reduced carbohydrate diet is an effective tool in the management in motivated obese patients with type 2 diabetes. The effect is generally retained after almost 2 years. A serving of grains is about half a cup.

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[ Diabetes Type 2 ]

Nutrition & Metabolism

イカスミで真っ黒です。 (Photo credit: Wikipedia) Black rice (Photo credit: Wikipedia Lots of natural foods & remedies are not promoted or even made known to the public simply because it’s against the commercial interests of the pharmaceutical corporations. It has quickly become known as a ‘super food’ and it’s also known as the “forbidden rice” according to the history books. The main difference between category ‘A’ and category ‘B’ is the harmful qualities typically present in ‘B’ items. It is also a key staple of a plant-based approach to eating, along with other whole grains, fruits, vegetables and legumes. For centuries it was called “forbidden rice” as it was reserved for the Chinese emperors due to its believed longevity attributes (Soleyman, 2010). If you’re trying to make a choice between the two, it’s helpful to look at how they stack up against each other nutritionally and in taste and texture. Of course, nearly 20 years of therapy and psychiatric medication pushed me along and helped the condition blossom.

Use this page as a cheat sheet alongside the book. These foods get a good press in the diabetes world because their digestion and absorption into the body is much slower and gentler thereby avoiding the spikes of high blood sugar. Xu said that brown rice is the most widely produced rice variety in the world. Richness of antioxidants in black rice can be proved with its purple or black colour. The dark color of black rice indicates the presence of powerful antioxidant-pigments called anthocyanins. The anthocyanin in the rice prevents plaques from forming in the arteries of the hearts. Check seasoning, and add salt if needed.

Anthocyanins are also known to play a role in controlling obesity and diabetes as they can inhibit digestive enzymes and hence reducing blood glucose levels. We hypothesized that black rice containing C3G may reduce the risk of hepatic fat accumulation and improve insulin resistance in high-fat diet-fed mice and tested this hypothesis in this study. McDougall:  “I want to to win the war rather than every battle”. With the supermarket shelves full of antibacterial sprays and cleaners you could be forgiven for thinking that bacteria are an enemy we have to destroy. In the liver, fatty acid oxidation occurs via mitochondrial and peroxisomal β-oxidation and microsomal CYP4A-catalyzed ϖ-oxidation [2, 27–29]. Heat a little olive oil in a saucepan and add finely sliced garlic. Therefore, to examine the mechanism underlying BRE inhibition of hepatic fat accumulation, we also measured the relative mRNA expression of PPAR-α, CPT1A, ACO, and CYP4A10 in the liver.

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[ Nutrition ]

Nutrition & Metabolism

Actoplus Met is a combination of metformin and pioglitazone. The ADA/EASD guidelines mention its use in patients irrespective of age, body weight and degree of baseline hyperglycaemia. Metformin acts to reduce hepatic gluconeogenesis and improve glucose uptake, and it may exert protective effects on pancreatic islet cells. Unfortunately, many of the traditional therapies for type 2 diabetes are associated with weight gain and hypoglycemia, resulting in poor compliance and subsequent worsening of glycemic control. -Note: There are saxagliptin-metformin combination products available internationally that contain immediate-release metformin; saxagliptin-metformin products containing immediate-release metformin should be dosed twice a day. Data were summarised under a random effects model. Ariane Godbout (Site PI), Michele Mahone (Site Co-I), Florence Weber (Site Co-I), Marie-Josee Bedard (Site Co-I), Bi Lan Wo (Site Co-I), and Sylvie Daigle (Site Coordinator), Centre Hospitalier de Université de Montréal, Hôpital St.

If you want a primer in diabetes, this is the best place to start. After exclusion of one study that investigated colorectal adenoma, the remaining four studies comprised 107,961 diabetic patients and 589 incident colorectal cancer cases during follow-up. At week 12, the mean change from baseline in HbA1c was 0.15% for MIR, 0.23% for MXR 1000 mg, and 0.04% for MXR 1500 mg. According to Currie, diabetics usually have to switch over to more aggressive treatments to control their condition. We recently evaluated the different effects of glipizide (a commonly used sulfonylurea) and metformin on the cardiovascular events and mortality in type 2 diabetic patients with coronary artery disease (CAD) in a multicenter interventional study (Study on the Prognosis and Effect of Anti-diabetic Drugs on Type-2 Diabetes Mellitus With Coronary Artery Disease [SPREAD-DIMCAD]) (7). Regarding the beneficial effect on metabolism of triacyglycerols, depression of the rate of VLDL-triacyglycerol secretion from the liver should be considered [7, 33]. Effective weight management is an essential component of the long-term treatment of type 2 diabetes (1).

First, it could explain why no effect on proteins linked to inflammation (anti – inflammatory cytokines, namely IL-1RA, IL-10, and pro-inflammatory cytokines, namely MCP-1, CRP, TNF-α, IL-6) was observed (Additional file 3), since metformin is known to exert anti-inflammatory action [3]. Indeed cytokine and adhesion molecule concentrations (cVCAM-1, sICAM-1, sE-selectin, sPECAM-1) were similar to those reported for healthy male subjects of different ages [34]. Importantly, no deleterious effects of any of the interventions on the markers of oxidative stress (SOD, TBARS, ratio GSSG/GSH) were observed (Table 1), possibly, due to the antioxidant effect of metformin [4]. Similarly, also insulin secretion remained unaffected by the interventions (see Results, Postprandial metabolism). Baseline characteristics were then compared using logistic regression or OLS regression, adjusted for octiles of the propensity score (online appendix table 1). In fact, Omega-3 alone marginally impaired markers of glycemic control (HbA 1c levels and fasting glycemia; Table 2 ) and glucose metabolism in the meal test (Fig. 4 ), but did not diminish insulin sensitivity (M) evaluated using a hyperinsulinemic-euglycemic clamp (Table 2 ).

These results are compatible with a model in which EPA + DHA per se do not deteriorate glucose utilization when glucose represents the main energy fuel (Fig. 5 , Clamp). Metformin also appeared to be the most effective medication for lowering levels of LDL (bad) cholesterol, according to the guidelines. In neither study, however, was insulin sensitivity directly measured. 5 , Fasting), glucose utilization is inhibited by multiple mechanisms involved in the Randle cycle (reviewed in [ 35 ]) reflecting the PPARα-mediated stimulation of fatty acid oxidation by EPA + DHA [ 12 ]. This would lead to the observed subtle deterioration of glucose metabolism by Omega-3. Metabolic changes in skeletal muscle, the main site of glucose utilization, probably play a major role.

That fasted glycemia is selectively increased by Omega-3 (Table 2 ) could also reflect increased hepatic gluconeogenesis stimulated in face of enhanced fatty acid oxidation [ 36 ]. Both decreased postprandial metabolism of glucose (Fig. 4 ) and elevated glycemia in fasted state could contribute to raised HbA 1c levels in the Omega-3 subgroup (Table 2 ). Forty-four subjects underwent vascular response measurements using forearm plethysmography (described in the following text) before and after three months’ treatment with metformin 500 mg orally twice daily or placebo. The negative effects of Omega-3 on glycemic control and glucose metabolism were prevented by Pio. Insulin sensitivity was increased by Pio&Omega-3, and tended to be improved by Pio compared with Omega-3 (Table 2), which is also in agreement with the induction of adiponectin by both Pio& Omega-3 and Pio (Table 1). These results were consistent with changes in metabolic flexibility to glucose evaluated using indirect calorimetry during the hyperinsulinemic-euglycemic clamp at week 24 (Fig.

3), since this parameter closely reflects whole-body glucose uptake [27]. And make sure that all your doctors know that you are pregnant, breastfeeding, or planning to get pregnant. Of some concern was the large number of patients who left the study, during follow-up but the reasons were mostly social and economic ones arising from repeated attendance at the clinic. In both the animal experiments and the present clinical trial, the robust PRCF analysis of RQ was used. This approach, which revealed here subtle differences in metabolic flexibility, has not been applied in humans before. Few studies were conducted to characterize possible modulation of metabolic flexibility by EPA + DHA in T2D patients, and very little is known about the effects of combined interventions using EPA + DHA and pharmaceuticals. La metformine pourrait constituer la première option thérapeutique dans le diabète de type 2 accompagné de surpoids ou d’obésité, car elle pourrait prévenir certaines complications vasculaires et réduire la mortalité.

Over a 9-week-period, dietary EPA + DHA exerted a transient improvement of glucose utilization followed by a shift from glucose to lipid catabolism, but the effect on metabolic flexibility is difficult to assess from these data since a relatively large volume (20 ml) of crude fish oil containing different lipid fractions besides EPA + DHA was used [38]. Thus, our study is unique regarding the use of a complex methodological approach including the indirect calorimetry, clamp as well as a meal test, which allowed us to demonstrate the additive improvements in metabolic flexibility to glucose, and namely in the postprandial lipid metabolism, by pioglitazone in combination with highly purified EPA + DHA.

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