Lipoic Acid: A Multitude of Metabolic Health Benefits. Given the rising epidemic of diabetes and its devastating complications, natural strategies that support healthy blood sugar (glucose) and protect against oxidative stress offer hope for many individuals. Metabolic syndrome—a combination of risk factors such as insulin resistance, high blood pressure, high triglycerides, and low high- density lipoprotein (HDL)—increases one’s risk for diabetes and cardiovascular disease. Widely known as a potent and effective antioxidant, lipoic acid demonstrates a multitude of unique properties. Regulated as a drug in several European countries (where it is approved for the treatment of diabetes- related complications, certain complications of alcoholism, and a variety of liver conditions),1,2 lipoic acid is an important component of every informed individual’s health maintenance regime. In emerging research, lipoic acid has shown impressive benefits in the context of glaucoma, migraine, stroke, as well as bone health. Protection Against Oxidative Stress. One of the underlying problems in diabetes is oxidative stress and the production of free radicals. These free radicals circulate in the body, attacking and damaging tissues. Since people with diabetes have high glucose levels, they are more prone to oxidative stress, which may contribute to the long- term complications of the disease. Antioxidants such as lipoic acid prevent this damage by neutralizing free radicals and reducing oxidative stress. Lipoic acid is an unusual antioxidant because it can act in both water- soluble and fat- soluble domains in cells and tissues. Thanks to these qualities, it is easily absorbed and transported into many organs and systems within the body, for example, the brain, liver, and nerves. Contrast this with antioxidants such as vitamin C, which is not very lipid- soluble (so is not able to penetrate the lipid wall of cell membranes very well), or vitamin E, which is not very water- soluble. When lipoic acid is combined with these antioxidants, the body’s ability to fight free radicals is greatly increased. In fact, lipoic acid helps to regenerate vitamins C and E. Furthermore, lipoic acid helps amplify the positive effects of other important antioxidants in the body such as glutathione and coenzyme Q1. It also teams with the B- vitamin family to support energy production in the body by converting the components of food, namely carbohydrates, proteins, and fats, into stored energy for future use. Lipoic acid does this by helping to protect mitochondria, the energy- producing factories of cells, from being damaged by oxidative stress, thus ensuring that energy production in the body remains efficient. Metabolic Syndrome and Diabetes. Overwhelming evidence now suggests that lipoic acid may be critical for not only maintaining optimal blood sugar levels by helping the body to use glucose, but also for supporting insulin sensitivity and key aspects of cardiovascular health, such as endothelial function. According to a just- released review of experimental studies, lipoic acid can help relieve several components of metabolic syndrome—a constellation of risk factors that often precedes full- blown types 2 diabetes. This review revealed that lipoic acid reduces blood pressure and insulin resistance, improves the lipid profile, and reduces weight. Scientists are encouraged by lipoic acid’s potential as a therapeutic agent for individuals with metabolic syndrome. Furthermore, another recent study of 3. L- carnitine reduced blood pressure and improved endothelial function of the brachial artery. This nutrient pair may therefore be an effective strategy for supporting healthy blood pressure levels, particularly in the context of metabolic syndrome. Just last year, investigators revealed dramatic effects of administering lipoic acid in improving insulin sensitivity in overweight adults suffering from type 2 diabetes. Lipoic acid produced significant improvements in a very short time frame—only four weeks of supplementation. This finding could have important implications, as insulin resistance lies at the heart of type 2 diabetes. Even after complications of diabetes have manifested, lipoic acid offers help. It has been found effective in the treatment of diabetic neuropathy, a type of nerve damage that occurs as a result of the toxic effects of high glucose levels on the nervous system in diabetes. Diabetic neuropathy is characterized by numbness, tingling, and pain best described as “burning” in the extremities. A large, randomized, placebo- controlled, multicenter, double- blind study involving 3. Although this early study was carried out using intravenous infusions of lipoic acid, later research has shown oral lipoic acid supplements to also be effective. Just five weeks of oral supplementation with lipoic acid significantly improved the stabbing pain, burning pain, and numbness of the feet in patients suffering from diabetic neuropathy, with the dose- effectiveness range being 6. The dose of R- lipoic acid to achieve this effect in diabetics would be half this amount, since it is the “R” form of lipoic acid that is biologically active in the body. Promoting Better Eye Health. Lipoic acid offers promise in supporting optimal visual health. As adults grow older, they become more vulnerable to developing cataracts, opacities of the lens that cloud sight. A key problem involved in cataract formation is oxidative stress in the lens of the eye. Lipoic acid was found to offer notable protection against cataract formation in an experimental animal model. Scientists believe that lipoic acid may confer this benefit by increasing levels of essential endogenous antioxidant enzymes such as glutathione peroxidase. Another common cause of vision loss is glaucoma. A study in patients with open- angle glaucoma found that visual function and other measures of glaucoma were improved in a group that received either 7.
Furthermore, a recent study revealed that the combination of lipoic acid and vitamin E helped prevent retinal cell death in animals with retinitis pigmentosa, an eye disease that also affects humans. As there is currently no effective medical treatment for this vision- robbing disease, the discovery of a nutritional approach to potentially treat retinitis pigmentosa is amazing news indeed. Neuroprotection. Given its strong ability to neutralize the damaging effects of oxidative stress, lipoic acid is the subject of intense study in preventing free radical damage to the neurological system. Lipoic acid is able to pass readily into the brain and reach all parts of a nerve cell. Experimental studies have shown that lipoic acid reduced brain damage after a stroke, and that those animals who received lipoic acid had a survival rate three times greater than those that did not. I have collected the following references to support the claims that, in those with PCOS: PCOS is associated with mood disorders including depression and bipolar. UDP-glucuronosyltransferase 1-1 also known as UGT-1A is an enzyme that in humans is encoded by the UGT1A1 gene. UGT-1A is a uridine diphosphate. Some of the protective effects conferred by lipoic acid in promoting healthy nerve function may be related to its ability to regenerate the antioxidant glutathione, which is often significantly depleted by harmful oxidative stress associated with cerebrovascular events such as stroke. New evidence also suggests that lipoic acid may help guard against one of the most dreaded conditions associated with aging—Alzheimer’s disease. Researchers have identified a series of mechanisms through which lipoic acid may work in helping prevent or manage Alzheimer’s disease. Scientists believe that lipoic acid may increase the production of acetylcholine, an essential nervous system messenger that is deficient in the brains of Alzheimer’s disease victims. In addition, preliminary works suggests that lipoic acid might be useful in those affected by multiple sclerosis. Investigators found that lipoic acid supplementation improved a variety of inflammatory measures that are associated with the disease. Further evidence also showed that lipoic acid supplementation produced improvements in animals suffering from an experimentally induced form of multiple sclerosis. Preserving Bone Density. Another area in which lipoic acid holds promise is in averting the bone loss that accompanies osteoporosis and other degenerative bone conditions. This multifaceted agent may help preserve bone health by quelling the oxidative stress that threatens to degrade healthy bone density. When applied to bone marrow cells and osteoblasts (bone- forming cells) in the laboratory, lipoic acid suppressed the formation of bone- degrading osteoclast cells in a dose- dependent fashion. It also reduced the process of inflammation- induced bone loss in both laboratory and living systems. Scientists believe that lipoic acid’s ability in preventing the loss of bone is linked to its inhibitory effects on pro- inflammatory prostaglandin E2 and the inflammatory cytokine tumor necrosis factor- alpha. These promising preliminary findings suggest a therapeutic role for lipoic acid in preventing and managing osteoporosis and other conditions that threaten bone density. Metal Chelation. Lipoic acid may also protect the body against toxic metal contaminants found in the environment and food supply. This multifunctional agent works by chelating these dangerous agents, such as arsenic, cadmium, lead, and mercury and rendering them inactive so that they can be removed by the body. In animal studies, lipoic acid has been shown to provide protection against arsenic poisoning and to safeguard the liver against the effects of cadmium exposure. Another study also showed that lipoic acid helped protect the delicate nervous system against the harmful effects of mercury poisoning. Migraine Prevention. Preliminary evidence suggests that lipoic acid could offer welcome relief for migraine sufferers. When a group of these individuals received a supplement of 6. Maintaining Healthy Skin. Among the myriad benefits of lipoic acid, scientists have found that it can also be used to improve the health of the skin. A study of 3. 3 women with an average age of 5. Using Lipoic Acid. Small intestinal bacterial overgrowth (SIBO) is a condition that is characterized by too many microorganisms in the small intestine. Unlike the large intestine or. Posted in Autoimmune Diseases, Blogs by Loren Cordain, Cooking, Digestion, Gluten Free, HP1, Inflammation, Metabolism, Paleo Diet Blog Articles, Politics What can our nutrient requirements, metabolism, and physiology tell us about what we should be eating? There are three broad theories about evolution and food. Systemic lupus erythematosus (SLE) is a multisystemic chronic inflammatory disease of unknown cause and autoimmune nature, characterized by the presence. Mary’s PCOS Treatment FAQ . Duke University Medical Center, Durham, North Carolina. PMID: 1. 53. 26. 42. Insulin resistance in depressive disorders and Alzheimer's disease: revisiting the missing link hypothesis. Rasgon NL, Kenna HA. Neurobiol Aging. 2. Dec; 2. 6 Suppl 1: 1. Epub 2. 00. 5 Oct 1. Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine. Several lines of evidence suggest an association between depressive disorders and Alzheimer's disease. AD). We previously suggested central nervous system (CNS) effects of insulin resistance (IR) to. AD. Although the exact mechanism of central. IR is not known, it is thought that central IR results in inadequate glucose metabolism in the brain. Further, in patients with undetected and/or untreated IR. Our studies. have demonstrated a high prevalence of IR in patients with depressive disorders, and reciprocally. IR disorder polycystic ovary syndrome. PCOS), and we believe these populations have significantly increased risk of cognitive decline. Mar; 1. 45(3): 3. Department of Psychiatry, School of Medicine, University of Pennsylvania, Philadelphia 1. An association between affective disorders and alterations in glucose utilization has been recognized. Depressed. patients demonstrated significantly higher basal glucose levels, greater cumulative glucose responses. GTT, and larger cumulative insulin responses after the GTT than control subjects. Values. for cumulative glucagon did not significantly differ between groups. These findings indicate the presence. PMID: 2. 89. 41. 76. A biochemical and functional characterization of diet- induced brain insulin resistance. Mielke JG, Taghibiglou C, Liu L, Zhang Y, Jia Z, Adeli K, Wang YT. J Neurochem. 2. 00. Jun; 9. 3(6): 1. 56. Brain and Behaviour Program, Hospital for Sick Children, Toronto, Ontario, Canada. While considerable research has examined diminished insulin responses within peripheral tissues, comparatively. CNS. The present study. FF). hamster. The tyrosine phosphorylation levels of the insulin receptor (IR) and insulin receptor substrate. IRS- 1) in response to insulin were significantly reduced within FF hamsters. Also, insulin- mediated. Akt/PKB, a key. effector of insulin signaling, was markedly decreased. Elevated levels of the protein tyrosine phosphatase. B, which dephosphorylates the IR and IRS- 1, were also observed within the cerebral cortex and hippocampus. FF hamsters. Examination of whether a nutritionally induced compromise of neural insulin signaling. Collectively. our results demonstrate, for the first time, that nutritionally induced insulin resistance significantly. PMID: 1. 59. 35. 07. The relationship between central serotonergic activity and insulin sensitivity in healthy volunteers. Horacek J, Kuzmiakova M, Hoschl C, Andel M, Bahbonh R. Psychoneuroendocrinology. Nov; 2. 4(8): 7. 85- 9. Faculty of Medicine, Charles University, Prague, Czech Republic. In order to determine whether central serotonin (5- HT) activity is related to sensitivity of insulin. Hb. Alc were studied. The relationship. D- fenfluramine (delta PRL) in a challenge test and metabolic clearance. MCR) of glucose during the hyperinsulinemic- euglycemic clamp technique was evaluated. Two levels of insulin concentration of approximately. U/l (MCRsubmax) and 2. U/l (MCRmax) were used in a clamp, each for a duration of 1. A negative. correlation was found between delta PRL and MCRsubmax (r = - 0. P < 0. 0. 2) and between delta PRL. MCRmax (r = - 0. 5. P < 0. 0. 3). We did not find any correlation between the prolactin response to. D- fenfluramine and body weight, body mass index (BMI) or waist and hip circumference (WHR). The data. support the hypothesis of a close connection between 5- HT activity in the brain and peripheral sensitivity. The possible physiological mechanisms of this connection are discussed. PMID: 1. 05. 81. 65. The metabolic syndrome is associated with reduced central serotonergic responsivity in healthy community. Muldoon MF, Mackey RH, Korytkowski MT, Flory JD, Pollock BG,Manuck SB. J Clin Endocrinol Metab. Feb; 9. 1(2): 7. 18- 2. Division of Clinical Pharmacology, Departments of Medicine and Epidemiology, University of Pittsburgh. CONTEXT: The pathobiology of the metabolic syndrome remains unclear. The central nervous system is. DESIGN, SETTING, PARTICIPANTS: This was a cross- sectional. OUTCOME MEASURES: Central serotonergic responsivity was assessed with. The serum prolactin area under the curve (AUC) over 1. The metabolic syndrome was defined according to the National Cholesterol Education Program. NCEP) and International Diabetes Federation (IDF) criteria. Insulin resistance was estimated by. RESULTS: Compared with other individuals, persons meeting either NCEP. IDF criteria for the metabolic syndrome had lower mean prolactin responses (P < 0. CONCLUSIONS: Corroborating previous evidence, the metabolic syndrome. This association may have implications for the etiology. PMID: 1. 63. 03. 83. Low central nervous system serotonergic responsivity is associated with the metabolic syndrome. Muldoon MF, Mackey RH, Williams KV, Korytkowski MT, Flory JD, Manuck SB. J Clin Endocrinol Metab. Jan; 8. 9(1): 2. 66- 7. Divisions of Clinical Pharmacology, Department of Medicine, University of Pittsburgh School. Medicine. The metabolic syndrome, recognized by the co- occurrence of general or abdominal obesity, hypertension. However, physiological processes linking the. The current study examined associations. The subjects were 2. Central serotonergic. PRL) response evoked by the serotonin- releasing agent. Across the sample, low PRL response was associated with greater body mass index. P < 0. 0. 3- 0. Finally, a 1 SD decline in. PRL response was associated with an odds ratio for the metabolic syndrome of 2. P = 0. 0. 02) and 5. P = 0. 0. 05), according. National Cholesterol Education Program and the World Health Organization. These findings reveal a heretofore unrecognized association between reduced central. PMID: 1. 47. 15. 86. Depressive symptoms, insulin resistance, and risk of diabetes in women at midlife. Everson- Rose SA, Meyer PM, Powell LH, Pandey D, Torrens JI, Kravitz HM, Bromberger JT, Matthews KA. Diabetes Care. 2. Dec; 2. 7(1. 2): 2. Department of Preventive Medicine, Rush University Medical Center, Chicago. OBJECTIVE: To examine depression and 3- year change in insulin resistance and risk of diabetes and whether. RESEARCH DESIGN AND METHODS: We analyzed data from 2,6. Caucasian, African- American. Hispanic, Japanese- American, and Chinese- American women without a history of diabetes from the Study. Women's Health Across the Nation. We estimated regression coefficients and odds ratios to determine. Center for Epidemiological Studies Depression Scale score > or =1. HOMA- IR) and greater risk of incident. RESULTS: Mean baseline HOMA- IR was 1. SD 0. 8. 6) and increased. P < 0. 0. 00. 1). A total of 9. 7 incident cases of diabetes occurred. The association between depression and HOMA- IR was eliminated. P=0. 8. 5). Depression predicted a 1. P < 0. 0. 3), which became nonsignificant after adjustment for central adiposity (P=0. We also observed. P < 0. 0. 5) in analyses limited to Caucasians and African Americans. Race- stratified models. African Americans only, after. P=0. 0. 08). CONCLUSIONS: Depression is associated with higher HOMA- IR values. These associations are mediated largely through. Nov; 5. 9(5): 5. 37- 5. Ramasubbu R. Department of Psychiatry, University of Calgary, Foothills Hospital, Canada. The association of depression with insulin resistance (IR) and athersclerotic vascular diseases has been. This review examines the relevance of IR as a link between depressive disorder and atherosclerotic. Relevant articles collected from Medline database over the period of 1. Studies have shown that IR is a state- dependent abnormality in depression and depression. Given that IR is a central component of cardiovascular. IR might play a role in the development and progression of coronary. Further, IR may contribute to the pathophysiology. In conclusion IR could account for the linkage between depression and atherosclerotic. More studies are needed to examine the importance of improving insulin sensitivity. PMID: 1. 23. 76. 07. Metabolism, mood and cognition in aging: the importance of lifestyle and dietary intervention. Hendrickx H, Mc. Ewen BS, Ouderaa F. Neurobiol Aging. 2. Dec; 2. 6 Suppl 1: 1- 5. Unilever Corporate Research, Colworth House, Sharnbrook MK4. LQ, UK. We are witnessing an unprecedented rise in obesity and Type 2 diabetes. Until recently, study of the. This paper summarizes. Spark workshop that focussed on the impact of obesity and diabetes on mood and cognition. Multiple mechanisms and mediators underlie this association including insulin, glucose. Importantly, prevention. In particular, increasing physical fitness and moderating/changing food. Prevention of obesity and hyperglycemia by adopting a healthy lifestyle. PMID: 1. 62. 90. 26. Alpha lipoic acid: a novel treatment for depression. Salazar MR. Med Hypotheses. Amherst College, Amherst, Massachusetts. Insulin resistance has been associated with people diagnosed with depression. Conversely, it has. Evidence suggests that insulin. In. accordance with the serotonin theory of depression, it may be possible to treat depression by increasing. The antioxidant alpha lipoic acid has been shown to increase insulin sensitivity and. Therefore, the nutrient alpha lipoic acid should be clinically. Copyright 2. 00. 0 Harcourt Publishers Ltd. PMID: 1. 10. 90. 30.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. Archives
May 2017
Categories |