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    • By Bursting Aura
      Here I reviewed some of the literature to give a better idea on whether we should be eating high-fat animal products for brain health. The underlying pathology of HPPD is in the brain. The fundamental things things we can do to improve brain health involves diet and nutrition. There is a large consensus that processed sugar products causes harm to the brain resulting in cognitive dysfunction. What is not clear is whether high-fat animal products are beneficial for brain health. The following literature provides some light on this confusing subject. 
      Exercise, Nutrition and the Brain
      Nutrition can also substantially influence the development and health of brain structure and function. Nutrition provides the proper building blocks for the brain to create and maintain connections, which is critical for improved cognition and academic performance. Dietary factors have a broad and positive action on neuronal function and plasticity. However, diets rich in sugar, saturated fats, or high in calories are considered deleterious for neural function, as they act to elevate levels of oxidative stress and to reduce synaptic plasticity and cognitive functions [4]. Brain function is certainly dependent on adequate nutrition, and short-term variations in the amount and composition of nutrient intake in healthy individuals influence measures of cognitive function. 
      Neuroinflammation has been proposed to be in the center of pathological alterations occurring in almost all age-related neurodegenerative diseases. Neuroinflammation has been correlated with neurodegeneration and cognitive decline.95–97 
      As described above, a number of factors have been proposed to cause high-fat diet-induced damage to the brain, especially with aging, including oxidative stress, insulin resistance, inflammation, and changes to vascularization/BBB integrity. The contribution of insulin resistance, essential fatty acid consumption, and oxidative stress may be coordinated with inflammatory and vascular alterations to cause overall changes in brain function with consumption of high-fat and high-glycemic index-type diets. 

      Diet-Induced Cognitive Deficits: The Role of Fat and Sugar, Potential Mechanisms and Nutritional Interventions
      Several interactive processes have been proposed to underlie cognitive decline related to poor diet including oxidative stress and inflammation [11], increased blood brain barrier permeability [12,13], reduced neurotrophic factors [14], and insulin insensitivity [15,16].
      Of concern is that a Western style diet high in saturated fat and refined sugars can impair certain types of memory in healthy subjects. Francis and Stevenson [31] for example showed that healthy undergraduate student participants with high self-reported fat and refined sugar intake were impaired on memory tasks that were sensitive to hippocampal function
      If we now focus on the macronutrient profile of the food, higher intakes of saturated fatty acids (SFA) have also been associated with cognitive impairment. Cross-sectional and longitudinal correlational studies indicate that higher intakes of SFA in young adulthood, mid and later life are associated with worse global cognitive function, impairments in prospective memory, memory speed and flexibility and an increased vulnerability to age related deficits and neurological diseases including dementia and Alzheimer’s disease 
      It is of vital importance to understand how foods which are making as fat, such as those high in saturated fat and refined sugar, also act to impair cognition and mood (potentially prior to weight gain), and how these deficits can further dysregulate appetite control.

      Damaging effects of a high-fat diet to the brain and cognition: A review of proposed mechanisms
      The major sources of SFAs in the United States include fatty meats, baked goods, cheese, milk, margarine, and butter.8,12,13. Long-term consumption of the ‘western diet’ can lead to obesity and consequently damaging effects on general health. However, an area that has not yet been well evaluated is the damaging effects of the ‘western diet’ on the brain. This topic is the focus of the current review.
      In human epidemiological studies, it has been shown that intake of a high-fat diet that includes mostly omega-6 and SFAs is associated with worse performance on a cognitive task.14,40–43 Furthermore, studies have shown that a diet containing mostly SFAs and TFAs is associated with increased risk for Alzheimer’s disease (AD).15,40,44 On the other hand, a lower fat diet consisting of omega-3 fatty acids had a protective effect against cognitive decline in healthy older subjects.45 It has also been determined that high consumption of total fats, SFAs, and cholesterol is associated with increased cholesterolemia, risk of cardiovascular disease, and impaired intellectual function, suggesting that the circulating levels of cholesterol are closely associated with cognitive performance in humans.46 Ortega et al.41 and Greenwood and Winocur23 have also found that high-fat diets and those that lack proper vitamins and minerals consumed late in life can worsen the course of age-related cognitive decline. 
      During the last decade, more studies have focused on biological mechanisms for these observed cognitive effects of high-fat diets. The major proposed biological mechanisms include insulin resistance, developmental disturbances, altered membrane functioning, oxidative stress, inflammation, and altered vascularization.32,33,35,45,47,48 A summary of the proposed mechanisms for high-fat diet-induced cognitive decline is presented in Fig. 1, and will be discussed in detail in the next section of this review.
      Obesity and neuroinflammation: A pathway to cognitive impairment
      Experimental studies have also provided insight into the potential mechanisms underpinning obesity-related cognitive dysfunction. For example, high fat feeding reduces synaptic plasticity in the hippocampus and cerebral cortex of rodents (Molteni et al., 2002; Wu et al., 2003; Stranahan et al., 2008b; Lynch et al., 2013), and there is evidence of increased neuronal apoptosis in the hippocampus and hypothalamus (Moraes et al., 2009; Rivera et al., 2013). In addition, high fat diet feeding of mice disrupts cerebral vascular function including neurovascular coupling, blood– brain barrier (BBB) permeability, and functioning of arteries upstream of the BBB (Li et al., 2013; Lynch et al., 2013; Pepping et al., 2013). Of importance, increasing evidence indicates that such vascular mechanisms are likely to be important components of the pathophysiological processes underlying vascular cognitive impairment and also AD (Gorelick et al., 2011).
      Obesity- and high fat diet-associated systemic inflammation was identified some time ago, with early reports suggesting obese humans and high fat diet-fed rodents have elevated circulating pro-inflammatory cytokines compared with controls, and macrophage infiltration into the WAT (Pickup and Crook, 1998; Weisberg et al., 2003; Wellen and Hotamisligil, 2003)
      1. Hypothesized mechanisms linking high fat diet/obesity and cognitive dysfunction. High fat diet and/or obesity lead to increased levels of circulating free fatty acids, pro-inflammatory cytokines, chemokines, and immune cells, which in turn gain access to the hypothalamus by increasing BBB permeability and/or via areas that lack an effective BBB (e.g. ARC).
      In addition to high fat per se influencing brain function, studies are now showing dietary composition is important in determining the central inflammatory profile. For instance, Maric and colleagues have recently demonstrated a diet high in saturated fats results in more hypothalamic inflammation after 8 weeks than one high in unsaturated fats (Maric et al., 2014). 
    • By Bursting Aura
      Some research I found on anti-depressants efficacy and comparisons with placebo. Worth a read.
       From Harvard
      Antidepressants and the Placebo Effect
      Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind. The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.

      The most commonly prescribed antidepressants are SSRIs, drugs that are supposed to selectively target the neurotransmitter serotonin. But there is another antidepressant that has a very different mode of action. It is called tianeptine, and it has been approved for prescription as an antidepressant by the French drug regulatory agency. Tianeptine is an SSRE, a selective serotonin reuptake enhancer. Instead of increasing the amount of serotonin in the brain, it is supposed to decrease it. If the theory that depression is caused by a deficiency of serotonin were correct, we would expect to make depression worse. But it doesn’t. In clinical trials comparing the effects of tianeptine to those of SSRIs and tricyclic antidepressants, 63% of patients show significant improvement (defined as a 50% reduction in symptoms), the same response rate that is found for SSRIs, NDRIs, and tricyclics, in this type of trial (Wagstaff, Ormrod, & Spencer, 2001). It simply does not matter what is in the medication – it might increase serotonin, decrease it, or have no effect on serotonin at all. The effect on depression is the same.
      What do you call pills, the effects of which are independent of their chemical composition? I call them “placebos.”
      From Duke and Brown University
      Antidepressants versus placebo in major depression: an overview
      As of now, antidepressant clinical trials have an effect size of 0.30, which, although similar to the effects of treatments for many other chronic illnesses, such as hypertension, asthma and diabetes, is less than impressive.
      Comparative benefits and harms of second-generation antidepressants for treating major depressive disorder: an updated meta-analysis.
      Meta-analyses and mixed-treatment comparisons of response to treatment and weighted mean differences were conducted on specific scales to rate depression. On the basis of 234 studies, no clinically relevant differences in efficacy or effectiveness were detected for the treatment of acute, continuation, and maintenance phases of MDD. 
    • By Bursting Aura
      Omega 3's are mentioned a lot for there importance for brain health. Vitamin D can also pass the blood-brain barrier, so it should be investigated for mental health also. I drove over some papers on vitamin D and depression since yesterday, so I will share some of those here. Depression impacts quality of life and it is usually implicated to be self-caused. According to science, depression can be biological, therefore depression is not always a lack of spiritual perspective or a case of "bad" vibes. My conclusion from these papers is that most cases of depression are very situational. Vitamin D deficiencies are not rare, and can potentially have a healing affect with some cases, similar to anti-depressants. The optimal ways to get vitamin D in my opinion, is sunshine and mushrooms. I would stay away from raw mushrooms due to carcinogens reported in the literature. heat destroys them though. https://www.ncbi.nlm.nih.gov/pubmed/2132000
      Efficacy of vitamin D supplementation in depression in adults: a systematic review protocol
      "The efficacy of vitamin D supplementation in depression has raised lots of concern. Vitamin D is considered as a neurosteroid [56], and now it is attested that vitamin D metabolites can cross the blood–brain barrier [34]. Because of the widespread presence of vitamin D receptor in areas of the brain including the hippocampus which is associated with the development of depression [23], it could be speculated that there is a clinical effect of vitamin D on depression."
      Vitamin D in anxiety and affective disorders.
      "Reduced levels of vitamin or its metabolites have been reported in various psychiatric disorders. Insufficient levels of vitamin D in depressive patients have been confirmed by many authors. Significantly lower levels of calcidiol (vitamin D) were found in men and women with depression as well as in age matched patients with anxiety disorders.
      Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior.
      "Serotonin regulates a wide variety of brain functions and behaviors. Here, we synthesize previous findings that serotonin regulates executive function, sensory gating, and social behavior and that attention deficit hyperactivity disorder, bipolar disorder, schizophrenia, and impulsive behavior all share in common defects in these functions. It has remained unclear why supplementation with omega-3 fatty acids and vitamin D improve cognitive function and behavior in these brain disorder"
    • By justaman
      I took hppd about 2 months ago and ever since I’ve been very aware of what I’m seeing. Like at night when I’m in the car driving, I’m not sure if it’s been there before but street lights or any sort of light kinda has a glare to it, like very shiny and has like a glow to it. I’ve noticed that when I look at the moon. There’s another moon next to it but half of the size, like a glare. I suck at explaining but am I getting hppd or is all this normal? I’ve been stressing over This for a while now and I’m going to a psychologist to get checked out. 
      I forgot to mention that I only taken lsd once. I’ve only smoked weed before . 
    • By HDDeer
      Hey guys,
      My doctor prescribed me lamictal yesterday and as pretty much all of you know, it's one of the more highly regarded medication out there for this condition.
      My hppd is actually very bearable, the only time I struggle is when I'm alone in the house where the lsd trip happened, which leads me to a few questions.
      If I decide to take it, and my hppd gets better/worse/stays the same, if I stop taking it will I return to baseline? Has anyone else taken this med? 
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Documentary about HPPD

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Hello everyone,

First of all, I'm really sorry for everyone here that suffers from HPPD, derealization, depersonalization, anxiety, depression, panic attacks and other symptoms. 

I'm a journalism student at Anglia Ruskin University, UK. As my final project, I'm making a documentary about HPPD as a way to raise awareness for this condition. 

I know about HPPD because of my boyfriend, he's been having it for almost 2 years now and this is my way of trying to understand him better and my way of trying to help in any way I can. 

For my documentary, I'd like to talk to other people with HPPD, because everyone experiences it differently. If any of you wouldn't mind sharing your story with me, you can contact me at this email - c.neves@outlook.pt

Your help would be truly appreciated.

Thank you so much in advance, 
Carolina Neves


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