Shown: posts 1 to 3 of 3. This is the beginning of the thread.
Posted by Netch on May 3, 2010, at 9:41:23
Low serum HDL-cholesterol levels are associated with long symptom duration in patients with major depressive disorder.
Aims: The purpose of the present study was to examine whether the association between depression and the serum high-density lipoprotein cholesterol (HDL-C) is modified by symptom duration. Methods: Depressed patients (n = 88) and an age- and sex-matched group of healthy general population controls (n = 88) underwent a Structured Clinical Interview for DSM-IV (SCID), and depressed participants reported the duration of their symptoms. The serum levels of total cholesterol (TC), HDL-C, low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and non-HDL, and the ratios of LDL-C/HDL and TC/HDL-C were assessed. Results: Major depressive disorder (MDD) subjects with a long symptom duration (>/=3 years) had lower levels of HDL-C compared with healthy controls or MDD subjects with a symptom duration <3 years. The likelihood for long symptom duration doubled for each 0.5-mmol/L decrease in HDL-C levels in regression models adjusted for age, gender, marital status, overweight, symptom severity, alcohol consumption, smoking, physical exercise, medication use, and non-HDL-C (P < 0.05). Conclusions: These findings suggest that a low serum HDL-C level, a risk factor for coronary heart disease, is specifically associated with long-term depressive symptomatology.
http://www.ncbi.nlm.nih.gov/pubmed/20374538
How can We Increase Our HDL Levels?
Posted by Phillipa on May 3, 2010, at 13:50:47
In reply to Low HDL associated with depression, posted by Netch on May 3, 2010, at 9:41:23
Don't get it makes no sense? Phillipa
Posted by desolationrower on May 7, 2010, at 21:33:38
In reply to Re: Low HDL associated with depression » Netch, posted by Phillipa on May 3, 2010, at 13:50:47
huh. not surpising i guess, hadn't seen them connected before though.
that list is pretty comprehensive, though increasing saturated fat (lauric, found in coconuts, has hte best HDL:total ratio of any fat http://www.ajcn.org/cgi/content/full/77/5/1146#SEC3), vitamin D, and dark chocolate are good too.
the interconnect is the same thing as mnetioned in jeroen's post a few posts away.
two studes just published in the last month, that i had open in my browser, and i wasn't even looking for mental health abstracts.
its only non-obvious because most people implicitly believe a strong dualism
Lipids and Cognition.
J Alzheimers Dis. 2010 Apr 22. [Epub ahead of print]
Lipids and Cognition.Morley JE, Banks WA.
GRECC, VA Medical Center and Saint Louis University School of Medicine, St. Louis, MO, USA.
AbstractCholesterol, omega-3 fatty acids, and triglycerides have been postulated to play roles in affecting cognition in Alzheimer's disease (AD), the elderly, and obesity. Animal, human epidemiological, and in vitro studies each suggest an important role for cholesterol in the regulation of amyloid-beta (Abeta) protein and the pathogenesis of AD. In contrast, well controlled studies have failed to show an effect of cholesterol lowering with statins on cognition, indicating that the cholesterol effect is spurious or indirect, possibly mediated through other lipids. Administration of diedocosahexanoic acid (DHA), a dietary omega-3 fatty acid derived primarily from fish and plants, improves cognition and reduces lipid peroxidation in animals, including in mouse models of AD. DHA also blocks Abeta-mediated tau phosphorylation. In humans, fish consumption or administration of DHA has been associated with cognitive improvement in many, but not all, studies. Both human and animal studies show that obesity is associated with cognitive impairments and that lowering triglycerides improves cognition. Administration of triglycerides to mice decreases learning and memory and impairs long-term potential. The effect of triglycerides may be mediated in part by inducing resistance to positive cognitive features of gastrointestinal hormones such as leptin. Overall, these studies strongly suggest that some lipids affect cognition in AD, the elderly, and obesity through a variety of mechanisms yet to be fully defined.
***
Prog Neurobiol. 2010 Apr 21. [Epub ahead of print]
EATING OURSELVES TO DEATH AND DESPAIR: THE CONTRIBUTION OF ADIPOSITY AND INFLAMMATION TO DEPRESSION.Shelton RC, Miller AH.
Vanderbilt University, 1500 21st Avenue South, Suite 2200, Nashville, TN 37212.
AbstractObesity and related metabolic conditions are of epidemic proportions in most of the world, affecting both adults and children. The accumulation of lipids in the body in the form of white adipose tissue in the abdomen is now known to activate innate immune mechanisms. Lipid accumulation causes adipocytes to directly secrete the cytokines interleukin (IL) 6 and tumor necrosis factor alpha (TNFalpha), but also monocyte chemoattractant protein 1 (MCP-1), which results in the accumulation of leukocytes in fat tissue. This sets up a chronic inflammatory state which is known to mediate the association between obesity and conditions such as cardiovascular disease, type 2 diabetes, and cancer. There is also a substantial literature linking inflammation with risk for depression. This includes the observations that: 1. People with inflammatory diseases such as multiple sclerosis, cardiovascular disease, and psoriasis have elevated rates of depression; 2. Many people administered inflammatory cytokines such as interferon alpha develop depression that is indistinguishable from depression in non-medically ill populations; 3. A significant proportion of depressed persons show upregulation of inflammatory factors such as IL-6, C-reactive protein, and TNFalpha; and 4) Inflammatory cytokines can interact with virtually every pathophysiologic domain relevant to depression, including neurotransmitter metabolism, neuroendocrine function, and synaptic plasticity. While many factors may contribute to the association between inflammatory mediators and depression, we hypothesize that increased adiposity may be one causal pathway. Mediational analysis suggests a bi-directional association between adiposity and depression, with inflammation possibly playing an intermediary role.
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