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      This is the catch-all forum for posts. Discuss anything related to Hallucinogen Persisting Perception Disorder (HPPD) here.

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      A place to introduce yourself to the community and what you hope to seek out on this site. New members may share their experience and onset of HPPD and what drug(s) triggered it.

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      What are the symptoms? What do you feel encompasses HPPD?

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      The place to discuss pharmacological and other treatment options.

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    1. Research Articles, Publications and Studies

      Articles, publications and studies for review and discussion.

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    1. Community Open Space

      This is a location to talk about anything except your symptoms. Be respectful of other users, but any topic within the rules are open for discussion.

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  • Hallucinogen Persisting Perception Disorder (HPPD) support forum - HPPD, flashbacks, drug-induced visual snow syndrome and depersonalization/derealization.

    Common HPPD symptoms: visual snow, palinopsia (trails/afterimages), increased BFEP, increased floaters, ghosting, halos, starbursts, macropsia/micropsia, geometric hallucinations, closed-eye visuals, flashbacks, depersonalization/derealization, anxiety, depression, brain fog, cognitive dysfunction, tinnitus.

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    • 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).     
    • Wow nice find. This information needs to get out there  
    • This could certainly explain mydriasis and a lot of the visual aspects of HPPD, but not all of course. What about DP, anxiety and all the other crazy mental stuff that goes along with it? I wonder if the nerve damage is widespread, effectively running from the eye to the back of the brain where other visual processing occurs. This could certainly explain the DP feeling of viewing the world from the far back of your head I guess... 
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