Category Archives: Medical Food

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NOVA Health Recovery | Alexandria, Va 22306 | Call for esketamine and nasal ketamine as well as IV Ketamine for depression, PTSD, anxiety  703-844-0184 < Link

Ketamine Virginia Link

What is interesting for the above articles is the Magnesium and copper components associated with Depression.

The most common biomarkers found are generally related to the regulation of lipid metabolism, control of immunoinflammatory response, control of vascular function, inter and intra-cellular communication. We additionally found that biomarkers related to nutrient sensing and proteostasis are related to LLD. Altogether, these studies suggest that there are core abnormalities, which are present in the first depressive episode, continue over mid-life and late-life, and are persistent even after successful antidepressant treatment. This view is consistent with the presence of biological “scars” in depression that render individuals with major depression , age, more vulnerable to systemic illness, disability, cognitive impairment and other negative health outcomes, which are not fully ameliorated despite successful antidepressant treatment . Robust machine learning techniques showed that three proteins (C-peptide, fatty acid-binding protein, and ApoA-IV) have a very high accuracy at discriminating individuals with remitted LLD compared to never depressed control participants. In fact, our study showed the highest discriminatory power of any previous studies, including those for schizophrenia, bipolar disorder or other common mental illnesses .

http://software.broadinstitute.org/gsea/msigdb

. LLD is associated with significantly higher levels of pro-inflammatory and lower levels of anti-inflammatory markers, reduced neurotrophic support, and higher levels of oxidative stress markers and activity of glycogen synthase kinase

I nflammation is a key pathway in the initiation and progression of coronary heart disease (CHD), and inflammatory biomarkers such as C-reactive protein (CRP) and interleukin-6 (IL-6) have shown consistent associations with incident CHD events (1). In recent years, myeloperoxydase (MPO) has drawn growing attention as a new inflammatory biomarker of CHD risk (2–4). Myeloperoxydase is an enzyme produced by activated leukocytes during the innate immune response that catalyzes the formation of reactive oxidant species. It is present in human atherosclerotic plaques and exhibits a variety of proatherogenic properties (5). Increased inflammation is a key mechanism through which several risk factors increase CHD risk (6). Depression is a risk factor for CHD (7), and whether increased inflammation is involved has attracted considerable interest (8). A role of inflammation in depression was first proposed by Smith in 1991 (9). Since then, several studies have reported a link between major depressive disorder (MDD) or depressive symptoms and a variety of inflammatory and immune biomarkers (10 –15). However, others have found no independent association (16) or mixed results (17–19), and one study even found lower levels of inflammatory biomarkers in depressed cardiac outpatients (20). It is increasingly recognized that the relationship between depression and inflammation is more complex than initially conceived (21). Depression may cause inflammation through altered neuroendocrine function and central adiposity (22). However, depression may also be a consequence of inflammation, since a pathogenic role of inflammatory cytokines in the etiology of depression has been described (23). Although given less consideration, a third possibility is that depression is a marker of some other underlying dimension that is separately linked to depression and inflammation. Recently, it has been proposed that such underlying factor could be a specific genetic makeup (24,25). Evidence for a common genetic substrate for depression and inflammation would be of substantial scientific and clinical interest, because it would suggest that a common biological pathway links these two conditions. We found that MDD is associated with higher levels of inflammation and that this association is particularly robust for MPO, an inflammatory biomarker that was never studied before in relation to depression. However, we also found evidence for genetic confounding in this association. Our results are consistent with the hypothesis that there is a common genetic substrate linking MDD and inflammation, suggesting that these two phenotypes share a common pathophysiological mechanism. MPO, Other Inflammatory Markers, and Depression Myeloperoxydase is an enzyme of the innate immune system, which exhibits a wide array of proatherogenic features (5,34). Myeloperoxydase is secreted upon leukocyte activation, contributing to innate host defenses. However, it also increases oxidative stress, thereby contributing to tissue damage during inflammation and atherogenesis. Myeloperoxydase generates numerous reactive oxidants that cause lipid peroxidation, posttranslational modifications to target proteins, and decrease of nitric oxide bioavailability, resulting in oxidation of LDL and apolipoprotein A1, protein carbamylation, and endothelial dysfunction (5,35,36). Transgenic mice containing the human MPO gene show significantly larger atherosclerosis buildup than the wild-type (34,37). In humans, individuals with total or subtotal MPO deficiency, a defect with a frequency of 1 in every 2000 to 4000 whites, are less likely to develop cardiovascular diseases, and those harboring a promoter polymorphism associated with a twofold reduction in MPO expression appear cardioprotected (5,38 – 40). Consistent with these proatherogenic properties, MPO has received growing attention as a novel risk marker for future cardiovascular events (2– 4). Oxidative stress has also been linked to neuronal degeneration in the central nervous system (41,42). Myeloperoxydase is both expressed and enzymatically active in the human brain (43,44) and is associated with Alzheimer’s disease (44). Previous studies have described abnormalities of oxidant-antioxidant systems in MDD suggestive of higher oxidative stress. For example, elevated levels of antioxidant enzymes, particularly superoxide dismutase (SOD), and biomarkers of oxidation, such as malondialdehyde, were found in plasma, red blood cells, or other peripheral tissues of acutely depressed MDD patients compared with control subjects (45– 47). In some cases (46,47), but not others (45), these abnormalities were reduced with antidepressant treatment. Superoxide dismutase coenzyme concentrations are also higher in postmortem brain tissue (prefrontal cortex) of MDD patients than in control brains (48).

MOOD FOOD Project

ADHD | Vayarin – Medical food for ADHD | 703-844-0184 | Addiction Treatment Center | Fairfax, Va 22306 | Ketamine Treatment Center | NOVA Health Recovery | Alexandria, Va 22306

ADHD | Vayarin – Medical food for ADHD | 703-844-0184 | Addiction Treatment Center | Fairfax, Va 22306 | Ketamine Treatment Center | NOVA Health Recovery | Alexandria, Va 22306

 

Vayarin – Medical food for ADHD

 

Vayarin Medical Food BROCHURE

 

 

 

A DRUG-FREE APPROACH TO MANAGING ADHD

Vayarin® is not a drug or a supplement. It is a medical food that is specially designed to provide important nutrients to the brain to manage specific lipid deficiencies associated with ADHD.

HOW DOES VAYARIN® REALLY WORK?

The Link Between FATS & ADHD

Lipids(fats) are critical for brain health. In fact, 60% of our brain’s dry weight is made of lipids!
Over time, humans have moved from being hunter-gatherers, to farming, to today’s industrial/high-tech era. The modern diet has resulted in a huge decrease of “healthy” lipids, such as Omega-3 fatty acids and phospholipids, which are very important to the brain.


Reduced levels of Omega-3s are also associated with ADHD. While nutrition may play a role, research show that dietary differences do not explain the deficiencies. Many factors like genetics, difficulty absorbing lipids, and other disturbances in breaking down fatty acids play a key role.


A DIFFERENT NEED, A DIFFERENT WAY

Vayarin® is a specially formulated lipid composition designed to target the brain, so that “healthy” lipids can get across the blood brain barrier.

Vayarin® is a nutritional approach to managing the lipid imbalance associated with ADHD – this is something that FDA-approved ADHD drug treatments do not address. Vayarin’s unique structure is different from dietary supplements or over-the-counter products in the market. Through a special patented process, we combine Phosphatidylserine (PS) and Omega-3, creating Eicosapentaenoic acid (EPA)-enriched PS-Omega-3, a composition that is designed to specifically travel to the brain and provide vital nutrients needed to manage the complex lipid deficiencies associated with ADHD. In a preclinical study comparing our PS-Omega-3 to common Omega-3s found in fish oil and PS, our composition was shown to have increased brain bioavailability. Don’t cheat your brain out of getting what it really needs!

 

SOLID SCIENCE

Vayarin® has been studied in a double-blind, placebo controlled, randomized clinical study in 162 children with ADHD, which was published in a peer-reviewed journal. The study demonstrated the safety of Vayarin® and, in the 15-week open-label extension phase evaluating efficacy, Vayarin® was shown to effectively reduce ADHD behaviors, especially in children with more emotional dysregulation. Additionally, in a retrospective study evaluating 518 patients with ADHD (average age 11), Vayarin® was shown to improve functioning and reduce emotional dysregulation.

Our unique PS-Omega-3 structure was shown to significantly increase the bioavailability of Omega-3 in rat brain versus control and fish oil alone, soy-PS and soy-PS combine with fish oil.