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Advanced General Psychology M3A2: Literature Review Remember Your Niacin: Hope for Alzheimer’s Disease M.L. Crider Argosy University March 21, 2018 Remember Your Niacin: Hope for Alzheimer’s Disease In my earnest hunt for articles that pinpoint information regarding niacin, vitamin B3, proving to be beneficial with respect to preventing or slowing Alzheimer’s Disease [AD], though there is a plethora of profound material available, I have selected fourteen sound and reliable references due to accessibility factors. Since AD is such a puzzling and dismal neurodegenerative disease, there is a tome of contributing factors that are beyond the scope of my intention for this work, and for which a book could surely and happily be scribed. In my brave attempt to offer some semblance of justice—or at very minimum, a fair voice—to the literal wealth of information contained in the fourteen articles I have now studied at length with biding and abundant hope that niacin will prove to be beneficial in the preclusion or slowing of getting AD, I commence below to summarize, compare, and discuss highlights of the articles. Some of the jargon forthwith is understandably medical or could best be understood by those in the epidemiological fields, but at this juncture in my studies I do attempt to summarize my understanding of the gist of each to the best of my ability. Dyslipidemia—high cholesterol or triglycerides [TG] that lead to atherosclerosis—was the focus of a study (Bowman, Kaye, & Quinn, 2012) that involved following thirty-six subjects for a year. This has great significance as it relates to the blood brain barrier [BBB]. They suggest that including niacin along with omega-3 in the diet could offer aid in bringing down harmful TG and cholesterol which in turn can aid in precluding AD. The strengths of this piece are how they explain the interconnectedness of niacin with AD but at the same time, the weakness would be that they do not delve into how niacin actually works, they just mention that it might. The following might elucidate this article’s mention of the role of the BBB with AD. “Dyslipidemia is more prevalent in AD subjects with BBB impairment. Plasma triglyceride and HDL cholesterol may have a role in maintaining BBB integrity in mild-to-moderate Alzheimer's disease. Extended-release niacin alters the metabolism of plasma apolipoprotein (Apo) A-I and ApoB-containing lipoproteins. The possibility that dyslipidemia is causally related to BBB impairment may be clinically significant since dyslipidemia is treatable […] While it is true that statin therapy has been unsuccessful in altering the course of AD, these current findings place emphasis on modifying triglyceride and HDL cholesterol, ideally in subjects selected on the basis of BBB impairment at baseline. Perhaps a dietary pattern or supplementation with omega-3PUFAs and niacin would offer one strategy, since they favorably modify triglyceride and HDL cholesterol metabolism, respectively. The emergence of imaging modalities for the assessment of BBB integrity will make these types of intervention more feasible. Blood-brain barrier dysfunction may have a significant role in the pathogenesis of Alzheimer's disease (AD) […] Plasma triglycerides explained 22% of the variance in BBB integrity and remained significant after controlling for age, gender, ApoE-4 genotype, blood pressure, and statin use. Dyslipidemia is more prevalent in AD subjects with BBB impairment. Plasma triglyceride and HDL cholesterol may have a role in maintaining BBB integrity in mild-to-moderate Alzheimer's disease” (Bowman, Kaye, & Quinn, 2012). The title of another article, “Niacin, an old drug, has new effects on central nervous system disease” (Chen & Chopp, 2010) promised more information…and it gave more information regarding niacin and its activity with regards to the hope of aiding with AD. It explained what niacin is in its elemental biological form that the body can use and how it is chief cousin to what we know to be nicotine—another short-term memory hero. It also connects the dizzying dots in great detail regarding how and why niacin plays an important role in preventing cognitive decline and AD more so than the Bowman, Kaye, & Quinn, 2012 article above. The strength of this article is that it goes to great length and a bit in layman’s terms for ease in understanding just how niacin truly works in the body. It sheds light on the specific differences between nicotinamide and niacin as well. “Niacin is converted to niacinamide—also known as nicotinamide […] Delayed treatment with nicotinamide inhibited brain energy depletion, improved cerebral microperfusion and protected hypertensive and hyperglycemic rats as well as wild type rats against a robust model of stroke. Nicotinamide also stimulates long-term survival and neuronal differentiation of chick embryo C cells. Nicotinamide offers multiple protective mechanisms in stroke as a poly (ADP-ribose) polymerase (PARP) inhibitor and by partial restoration of mitochondrial function […] Niacin not only regulates cholesterol levels but is also converted to nicotinamide, which encourage the possible use of niacin and nicotinamide as a therapeutic neuroprotective and neurorestortive agent in the clinical treatment of ischemic stroke […] Niacin and nicotinamide are water-soluble B complex vitamins. Niacin is converted to nicotinamide, a constituent of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) in vivo, which are coenzymes involved in glycogenolysis, tissue respiration and lipid metabolism. Niacin is metabolized in the liver to nicotinamide. Nicotinamide is widely distributed in the body. Nicotinic acid and nicotinamide can penetrate the blood brain barrier. Although the Niacin and nicotinamide are identical in their vitamin activity, nicotinamide does not have the same pharmacological effects as niacin, and does not reduce cholesterol, increase HDL cholesterol or cause flushing. Nicotinamide, the amide form of Niacin, is the precursor for the coenzyme beta-nicotinamide adenine dinucleotide (NAD+) and is considered to be necessary for cellular function and metabolism. Nicotinamide also plays an important role on regulation of both neuronal and vascular cell populations in the brain injury […] Total cholesterol and LDL are significantly related to pathologically defined Alzheimer Disease. High serum cholesterol levels induce the elevation of brain Apolipoprotein E, which plays a role in aggravating the Abeta accumulation. Merched et al. have shown that ApoAI levels were significantly lower in Alzheimer Disease patients and were highly correlated with mini-mental state scores of Alzheimer Disease patients. In addition, cellular cholesterol modulates axon and dendrite outgrowths and neuronal polarization, and cellular cholesterol homeostasis are causally involved in different steps leading to pathological events in the brain of Alzheimer Disease patients. Cellular cholesterol levels modulate Abeta generation, whereas Abeta alters cholesterol dynamics in neurons, leading to tauopathy. Abeta is formed from the amyloid precursor protein (APP) in cholesterol-enriched membrane rafts, and cellular cholesterol depletion decreases Abeta formation. Increasing membrane cholesterol in immature neurons might render mature hippocampal neurons sensitivity to -amyloid (A)-induced calpain activation and tau toxicity. In addition, the risk of amyloid deposition associated with high cholesterol may be through induction of the Liver X receptors (LXR) system […] T0901317, a LXR agonist, decreases amyloidogenic processing of APP in vitro and in vivo. LXR agonists facilitate the clearance of Abeta42 and represent a novel therapeutic approach to Alzheimer's disease. Niacin up-regulates LXR-alpha and peroxisome proliferator-activated receptor gamma (PPARgamma) mRNA expression and promotes the HDL-induced cholesterol efflux. Therefore, niacin decreases serum and cellular cholesterol levels, which may play a role on protection of Alzheimer's disease. Dietary niacin regulates learning performance, and prevents or reverses cognitive decline, protects against Alzheimer Disease and age related cognitive decline. Dietary niacin has been implicated as a protective factor against cognitive decline and Alzheimer's disease” (Chen & Chopp, 2010). Another interesting article (Chowdhury & Kumar, 2017) focused on spices and niacin being an excitor in the way of keeping neurons alive and active. For whatever reason, it listed niacin as a spice. I am unclear if language barrier that is lost in translation between languages when translating to English is culprit or not. That would be its weakness in that it is unclear why they added niacin to their list of spices. It tries to introduce using spices as an alternative method for keeping synaptic plasticity and neuronal survival in tact. The strengths might include its focus on phytocompounds found in spices and niacin prove to show potent antagonist properties when it comes to NMDA. This, they believe is promising with regards to preventing AD. I also quite appreciate its slant or bias, with regards to my inquiry about niacin, with regards to the pharmaceutical industry not positing enough results when it comes to solving the puzzle of preventing or slowing AD. “N-methyl-d-aspartate receptor (NMDAR) play key role in glutamatergic neurotransmission which is critical for synaptic plasticity and survival of neurons. However, ‘slow excitotoxicity’ at post- synaptic neurons promotes gradual neurodegeneration as occurred in Alzheimer’s disease (AD). In view of this natural and synthetic compounds that act as antagonist against NMDA receptor considered as potential target in AD. The present study explores various spices phytoconstituents such as Piper nigrum, Cinnamomum zeylanicum, Eugenia caryophyllus, Cuminum cyminum and Eletteria cardamom as a potential source of novel NMDA receptor antagonist […]Out of 240 compounds analyzed Caffeic acid, Cinnamic acid, Octanoic acid, Capric acid, Valeric acid, Palmitic acid, Sotolone, Niacin, Butanoic acid and Dehydrodieugenol were the top 10 leads […] Higher numbers of conformations, low docking score and the lowest binding energy indicated better affinity of the compounds to the NMDA receptor. Owing to the diverse and rich source of plants, use of herbs and spices as medicine dates way back in history. Due to side-effects of drugs, phyto-constituents have gained enormous consideration as an alternative. The phytocompounds from spices showed potent NMDA antagonist property and provides a lead towards finding more potent anti-Alzheimer's drug” (Chowdhury & Kumar, 2017). In another (Fu, Doreswamy, & Prakash, 2014) article, we look into the deficiency of niacin leading to neural degeneration in the central nervous system [CNS] It speaks of how biochemical pathways might be involved in neural degeneration and it boasts that this is a fact supported in many substantive studies. It claims that niacin is a necessity in a number of biochemical pathways. It tries to distinguish between plain degeneration due to environmental factors, i.e. diet, and primary neurodegenerative disorders such as AD perhaps being partially caused by genetic pathogens. They claim that much is unknown and they repeat such with seeming intent to bolster our faith in their trial that aims to distinguish between normal niacin deficiency and the pathogenic genetic component. Its strength is how it breaks down how niacin works as well as differentiating the differences between niacin and nicotinamide as does the Chen & Chopp, 2010 article above; its weakness is how it leaves a branded question mark’s ghost watermarked all over its insecure compilation. “Over past few years, some prominent biochemical pathways which are disturbed in niacin deficiency and possibly contribute to the neurodegenerative events have been identified. However, we could not find any literature where these pathways have been reviewed together […] Neural degeneration is a very complicated process. In spite of all the advancements in the molecular chemistry, there are many unknown aspects of the phenomena of neurodegeneration which need to be put together. It is a common sequela of the conditions of niacin deficiency […] There is a gross lack of understanding of biochemical mechanisms of neurodegeneration in niacin deficiency states. Because of the necessity of niacin or its amide derivative NAD in a number of biochemical pathways, it is understandable that several of these pathways may be involved in the common outcome of neural degeneration. Here, we highlight five pathways that could be involved in the neural degeneration for which evidence has accumulated through several studies. These pathways are: 1) the tryptophan-kyneurenic acid pathway, 2) the mitochondrial ATP generation related pathways, 3) the poly (ADP-ibose) polymerase (PARP) pathway, 4) the BDNF-TRKB Axis abnormalities, 5) the genetic influences of niacin deficiency […] Niacin is chemically synonymous with nicotinic acid although the term is also used for its amide derivative (nicotinamide). Nicotinamide is the form of the vitamin, which does not have the pharmacological action of the acid. It is the amide form that exists within the redox-active co-enzymes, nicotinamide adenine dinucleotide (NAD) and its phosphate (NADP), which function in dehydrogenase-reductase systems requiring transfer of a hydride ion […] In the chemical form of NAD, niacin is involved in a number of biochemical processes, including energy metabolism (redox reactions), protein modification by mono and poly (ADP-ribose) polymerases and synthesis of intracellular calcium signaling molecules […] NAD is also required for non-redox adenosine diphosphate-ribose transfer reactions involved in DNA repair and calcium mobilization. It also participates in intracellular respiration along with enzymes involved in the oxidation of fuel substrates such as glyceraldehyde 3-phosphate, lactate, alcohol, 3-hydroxybutyrate, and pyruvate. NADP mainly functions in reductive biosynthesis such as fatty acid and steroid synthesis and in the oxidation of glucose-6-phosphate to ribose-5-phosphate in the pentose phosphate pathway. Neurodegenerative pathology in niacin deficiency is well-known” (Fu, Doreswamy, & Prakash, 2014). In the (Kapogiannis & Mattson, 2010) article, the researchers dive into energy metabolism disruption and neuronal circuitry dysfunction with respect to the cognitive impairment of those with AD. This piece focuses on the adaptation of neurons to stress. It isn’t the strongest article just because it seems so much more has been found since 2010 than what it proffers. However, it would parle nicely with any of the other articles I am studying and perhaps help to carve the key that unlocks the rusty door of the correlation of niacin aiding in AD. “Ageing and Alzheimer's disease cause perturbations in cellular energy metabolism, level of excitation or inhibition, and neurotrophic factor release, which overwhelm compensatory mechanisms and result in dysfunction of neuronal microcircuits and brain networks. A prolonged positive energy balance impairs the ability of neurons to adapt to oxidative and metabolic stress. Results from experimental studies in animals show how disruptions caused by chronic positive energy balance, such as diabetes, lead to accelerated cognitive ageing and Alzheimer's disease. Therapeutic interventions to allay cognitive dysfunction that target energy metabolism and adaptive stress responses (such as neurotrophin signalling) have been effective in animal models and in preliminary studies in humans” (Kapogiannis & Mattson, 2010). The (Mangialasche, 2010) article in a highly generalized uncourageous fashion acts as a town crier in its meek call to pharmaceutical companies, basic researchers, and clinical researchers to please collaborate and come up with roses in the boggling quagmire that is AD. It is one of the weaker articles I have delved into due to its generality while my sole aim is more specificity with regards to niacin’s effects on the body/brain connection of AD. “Alzheimer's disease is the most common cause of dementia in elderly people. Research into Alzheimer's disease therapy has been at least partly successful in terms of developing symptomatic treatments, but has also had several failures in terms of developing disease-modifying therapies. These successes and failures have led to debate about the potential deficiencies in our understanding of the pathogenesis of Alzheimer's disease and potential pitfalls in diagnosis, choice of therapeutic targets, development of drug candidates, and design of clinical trials […] We need to acknowledge that a single cure for Alzheimer's disease is unlikely to be found and that the approach to drug development for this disorder needs to be reconsidered” (Mangialasche, 2010). This (Monte, 2012) article claims that we have spent a long and hard thirty-plus years trying to get to the bottom of AD and that AD is the most common cause of dementia in North America. It also claims that AD is a metabolic disease kin or similar to diabetes, but does not go into how or why. This article, like the Mangialasche, 2010 article, seems to point to others to further elaborate on untying the knots of the causation and therapeutic remedies due to AD. It does not focus on niacin, save that it does mention components that are mentioned in articles that do focus on niacin’s role in possibly preventing AD. A strength is that it does bring up information regarding the connection of hyperphosphorylated tau and AD. “Growing evidence supports the concept that AD is fundamentally a metabolic disease with substantial and progressive derangements in brain glucose utilization and responsiveness to insulin and insulin-like growth factor [IGF] stimulation. Moreover, AD is now recognized to be heterogeneous in nature, and not solely the end-product of aberrantly processed, misfolded, and aggregated oligomeric amyloid-beta peptides and hyperphosphorylated tau. Other factors, including impairments in energy metabolism, increased oxidative stress, inflammation, insulin and IGF resistance, and insulin/IGF deficiency in the brain should be incorporated into all equations used to develop diagnostic and therapeutic approaches to AD […] The contributions of impaired insulin and IGF signaling to AD-associated neuronal loss, synaptic disconnection, tau hyperphosphorylation, amyloid-beta accumulation, and impaired energy metabolism are reviewed […] It is imperative that future therapeutic strategies for AD abandon the concept of uni-modal therapy in favor of multi-modal treatments that target distinct impairments at different levels within the brain insulin/IGF signaling cascades” (Monte, 2012). (Morris et al., 2004) I have a winner in this article! Like the research done by UHN Staff, 2017 and the Sealey, 2017 articles below herein, it specifies the testing of niacin and its effects on AD and cognitive decline prevention. It, like the final articles that follow, braves the waters with specificity in the realm of this subject matter. Additionally, in the way of strengths, it seems that the researchers went to great lengths to be fair in their testing variables in order to achieve valid results. This article’s confidence in its results is reassuring with regards to taking niacin for brain/body health and its association with niacin’s positive effects. These findings are anything but weak; they aim at speaking the truth simply about such a subject wrought with complication. “The protective association was specific to niacin intake as opposed to other related B vitamins […] We also found a specific protective effect of niacin intake from food against 6-year cognitive decline among 3718 participants in the larger cohort that was only strengthened in sensitivity analyses excluding participants with low initial cognitive scores or with less than a high school education, and with control for dietary and other potential confounders […] In this prospective population based study, we observed inverse associations between AD and dietary intakes of total niacin (foods and supplements), niacin from foods only, and tryptophan. Although participants in the lowest fifth of intake had the greatest risk of AD, a statistically significant log linear inverse association remained when we restricted the analyses to participants with higher intake levels. Higher intake of niacin from food sources was also linearly associated with lower cognitive decline in the study population. The protective association of niacin against AD was observed after controlling for the important risk factors for dementia (age, education, race, ApoE e4) as well as many other dietary and non-dietary factors that could potentially account for the results […] Niacin intake from foods was also inversely associated with AD” (Morris et al., 2004). This (Qin et al., 2017) article highlights specific kinds of memory testing and for this it is strong. Its specificity regarding what the researchers found with regards to niacin intake and cognition proves winsome and on target. They examine diet history and run a barrage of different cognitive tests and show the positive effects of niacin. The weakness in the scope of my paper is that the medical jargon makes it difficult to truly absorb regarding their findings, unless of course, one is adept to interpreting works within the medical field. “Epidemiologic evidence regarding niacin, folate, vitamin B-6, and vitamin B-12 intake in relation to cognitive function is limited, especially in midlife. Objective: We hypothesize that higher intake of these B vitamins in young adulthood is associated with better cognition later in life […] We examined participants’ CARDIA diet history at years 0, 7, and 20 to assess nutrient intake, including dietary and supplemental B vitamins. We measured cognitive function at year 25 (mean ± SD age: 50 ± 4 y) through the use of the Rey Auditory Verbal Learning Test (RAVLT) for verbal memory, the Digit Symbol Substitution Test (DSST) for psychomotor speed, and a modified Stroop interference test for executive function. Higher RAVLT and DSST scores and a lower Stroop score indicated better cognitive function. We used multivariable-adjusted linear regressions to estimate mean differences in cognitive scores and 95% CIs. Results: Comparing the highest quintile with the lowest (quintile 5 compared with quintile 1), cumulative total intake of niacin was significantly associated with 3.92 more digits on the DSST” (Qin et al., 2017). The (Reitz, 2012) article would be helpful for a doctor or those in the epidemiological fields, but it, like the UHN Staff, 2017 article, pinpoints the glory of nicotinamide and notes its stabilizing factors. Like the Monte, 2012 article, it whispers about the important connection between phosphorylated tau and AD again. It makes note of its safe use in clinical studies and especially those that target outcomes for people with neurodegenerative disorders such as AD. Its hyper focus on nicotinamide makes it a sound resource with regards to providing true hope in the dismal muddy search for promise of some kind of honest cure for AD. “Nicotinamide is the biologically active form of niacin (vitamin B3) and the precursor of coenzyme NAD+. Orally administered nicotinamide can prevent cognitive deficits in a mouse model of AD and can reduce brain concentrations of a species of phosphorylated tau (Thr231) that inhibits microtubule polymerization. Furthermore, nicotinamide inhibits brain sirtuin deacetylase and upregulates acetyl-α-tubulin, protein p25, and MAP2c; all these interactions are associated with increased microtubule stabilization. Nicotinamide has been used in several clinical studies, including RCTs in patients with neurodegenerative disorders, and is generally safe and well tolerated” (Reitz, 2012). This (Sealey, 2017) is an article about a book that wants the public to know about the immense success that a certain Dr. Hoffer had with treating thousands of patients with niacin. The fact that he treated thousands of patients with niacin and it seemed to better their conditions (long before Big Pharma ransacked the health scene) is plain and simple promise indeed! It is a niacin cheerleader resource. It claims that niacin helped his patients to live longer and enjoy a better way of life. It tries to justify the clinical use of niacin via recovery stories and testimonies. Its weakness would be that it doesn’t get into how niacin works, but other articles in my resources herein provide this information in spades and so it complements nicely to the larger picture for us. It is noteworthy that long before the bad politics became a thicket with Big Pharma deep pockets and the health industry, that a doctor was afforded to be so bold as to prescribe his patients niacin. Bravo to him! Nowadays, doctors don’t prescribe vitamins, they suggest them, if they are good doctors. Heck, American doctors are rarely even required to take courses on nutrition in this modern day—as if nutrition should be separated from health! Alternative medicine doctors now prescribe vitamins and herbs to their patients. I respect this article about the brave doctor who proved to help thousands, yes, thousands, recover. “Abram Hoffer, Andrew Saul and Harold Foster wrote Niacin: The Real Story to inform the public that niacin (vitamin B3) has a broad spectrum of healing properties. Decades of research and clinical practice taught Dr. Hoffer that optimum doses of niacin can treat mental, cardiovascular, arthritic and other illnesses. When he prescribed vitamins, many patients recovered. Hoffer, Saul and Foster’s book explains what niacin is, when niacin therapy began, how niacin works, why we need more niacin, how to take niacin and why niacin is safe. It introduces doctors who prescribe niacin and other vitamins and references their books. During his 60-year career, Dr. Hoffer gave niacin to thousands of patients. His finding? Niacin helped patients feel better and live longer. This book provides research reports and recovery stories which justify the clinical use of niacin for mental illness and cardiovascular problems and niacinamide for arthritis. A long chapter outlines how patients with 25 other health problems also respond well to vitamin B3 therapy. The only cautionary note concerns niacin’s harmless and noticeable but short-lived flush effect” (Sealey, 2017). This (Thoenes et al., 2007) article’s focus is on inflammation and arterial thickness with relation to niacin. It also delves into the metabolic action of niacin after testing fifty patients for fifty-two weeks. It supports niacin’s significance in the health and medical fields. Its only weakness would be that it doesn’t necessarily focus on AD, but since AD is such a knotted mystery to most due to the interrelatedness of many factors that can lead to AD, I find this article most useful in my earnest quest in collecting the mysterious pieces that lead to AD. “Niacin is an agent that significantly increases high-density lipoprotein cholesterol (HDL-C), but its effects on surrogate markers of atherosclerosis and inflammatory markers are less clear. We studied the effects of niacin on carotid intimal media thickness (IMT), brachial artery reactivity as well as markers of inflammation and the metabolic profile of patients with metabolic syndrome […] Fifty patients with the metabolic syndrome (Adult Treatment Panel (ATP) III criteria) were randomized to either extended-release niacin (1000 mg/day) or placebo. After 52 weeks of treatment, there was a change of carotid IMT of +0.009 ± 0.003 mm in the placebo group and −0.005 ± 0.002 mm in the niacin group (p = 0.021 between groups). Endothelial function improved by 22% in the group treated with niacin” (Thoenes et al., 2007). As mentioned with affection throughout above, this (UHN Staff, 2017) piece is a fantastic collaborative article that boasts the memory protection of B vitamins and niacin in a painstaking and successful fashion. It flat-out states that niacin plays a significant role in protection against AD and that a deficiency in Bs and niacin show cognitive decline, no question. It introduces the idea that treatment with B vitamins after two years not only prevented cognitive decline but also reduced atrophy and actually slowed down shrinkage of the entire brain! What I like most about this article is that it states that niacin is an active agent in DNA synthesis and repair while it also makes the connection between niacin preventing AD due to it making the body’s good cholesterol and lowering the bad cholesterol. It states these things with confidence and after testings that seem to hold validity amongst the researchers’ peers. “Among the many supplements and vitamins for memory protection are the B-vitamins, including B12, B6, B9, and B3, or niacin. While the first two are more commonly associated with dementia and cognitive function, niacin benefits the brain as well, and it may play an important role in protecting against Alzheimer’s disease. B Vitamins for Memory Loss and Dementia Most attention on B vitamins for dementia focuses on vitamin B12, B6, and B9. This isn’t surprising; studies show that deficiencies in these vitamins are common in the elderly and can contribute to cognitive decline. Treatment with a complex of B-vitamins helps to prevent neurodegeneration. One study showed that over two years, vitamin B treatment slowed shrinkage of the whole brain, and further study showed that B vitamins reduced gray matter atrophy in regions of the brain specifically susceptible to Alzheimer’s-related degeneration. Niacin Helps Prevent Alzheimer’s. Niacin treatments have led to improvements in cognitive test scores and overall function, while a deficiency in niacin (called pellagra) can cause symptoms of mental confusion and dementia, along with scaly skin, muscle weakness, and diarrhea. One study found that lower blood levels of niacin were more common among elderly patients with dementia than controls. A large study in the Journal of Neurology, Neurosurgery, and Psychiatry looked at niacin intake and Alzheimer’s disease incidence in more than 6,000 people. The researchers found that those with the highest total intake of niacin were much less likely to get Alzheimer’s disease. Niacin intake through food sources was also inversely associated with Alzheimer’s risk. The study also showed that high food intake of niacin was associated with slower rate of cognitive decline. The authors conclude that “dietary niacin may protect against Alzheimer’s disease and age related cognitive decline.” Niacin is important for DNA synthesis and repair, the growth and formation of nerve cells, cell signaling, and antioxidant functions in the brain, all of which likely contribute to the niacin benefits for dementia. Niacin is also one of the more effective ways to lower bad cholesterol and raise good cholesterol. It turns out that cholesterol levels are linked to Alzheimer’s disease, so another way niacin may prevent Alzheimer’s is through keeping cholesterol in check” (UHN Staff, 2017). Finally, the (Williams, Plassman, Burke, Holsinger, & Benjamin, 2010) article contrasts the B vitamins and their roles, functions, power, and lack of power to prevent AD. Niacin is made a winner of the Bs specifically for preventing AD as their results show that a higher intake of niacin proves to lower the risk of getting AD. The strength of this article is that it differentiates between the B vitamins and crowns niacin as the necessary one in the prevention of AD. “Results from the two studies that measured folate serum levels showed that low baseline folate levels were consistently associated with increased risk of AD (or dementia). In comparison, B12 levels were typically not associated with risk of AD. The three studies that used estimated dietary intake of folate and B vitamins based on self-reported information reported conflicting results. One reported an association between higher intake of folate and reduced risk of AD, while another did not find a significant reduction in AD risk associated with folate intake. Neither study found an association between vitamins B6 or B12 and risk of AD. Direct comparisons of the two studies to identify reasons for these inconsistent results are difficult, but based on the information provided in the studies, the average rate of folate intake may differ between the two studies […] Only one study examined niacin (B3) intake and found a lower risk for AD associated with higher intake of niacin. In conclusion, based on folate levels measured in serum, there is preliminary evidence from two studies that low folate levels are associated with increased risk of AD. The two studies estimating folate level from self-report dietary information did not find a consistent association with risk of AD. The evidence does not suggest an association between B12 and risk of AD. The one study assessing estimated niacin intake showed an association between higher niacin intake and lower risk of AD […] One study examined the association between niacin (B3) and cognitive change over time. Investigators reported that higher dietary intake of niacin was generally associated with a modest protective effect on cognition; however, the results were only significant in subgroups of individuals without stroke or myocardial infarction or individuals with baseline cognitive scores in the upper 85 percent of the sample” (Williams, Plassman, Burke, Holsinger, & Benjamin, 2010). References Bowman, G. L., Kaye, J. A., & Quinn, J. F. (2012, May 13). Dyslipidemia and blood-brain barrier integrity in Alzheimer's Disease. Retrieved from https://www.hindawi.com/journals/cggr/2012/184042/abs/ Chen, J., & Chopp, M. (2010). Niacin, an old drug, has new effects on central nervous system disease. The Open Drug Discovery Journal, 2, 181-186. Retrieved from https://pdfs.semanticscholar.org/ae7c/cd3370e3da8d0b41ea376f55a6887d0439c2.pdf Chowdhury, S., & Kumar, S. (2017, July). Identification of novel NDMA receptor antagonist from spices: A molecular docking study. Retrieved from http://www.alzheimersanddementia.com/article/S1552-5260(17)30394-1/fulltext Fu, L., Doreswamy, V., & Prakash, R. (2014, August 15). The biochemical pathways of central nervous system neural degeneration in niacin deficiency. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4192966/ Kapogiannis, D., & Mattson, M. (2010, December 10). Disrupted energy metabolism and neuronal circuit dysfunction in cognitive impairment and Alzheimer's disease. Retrieved from https://www.sciencedirect.com/science/article/pii/S1474442210702775 Mangialasche, F. (2010, June 16). Alzheimer's disease: Clinical trials and drug development. Retrieved from https://www.sciencedirect.com/science/article/pii/S1474442210701198 Monte, S. M. (2012, January). Brain insulin resistance and deficiency as therapeutic targets in Alzheimer's Disease. Retrieved from http://www.ingentaconnect.com/content/ben/car/2012/00000009/00000001/art00004 Morris, M., Evans, D., Bienias, J., Scherr, P., Tangney, C., Hebert, L., . . . Aggarwal, N. (2004, August). Dietary niacin and the risk of incident Alzheimer's disease and of cognitive decline. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1739176/ Qin, B., Xun, P., Jacobs, D. R., Zhu, N., Daviglus, M. L., Reis, J. P., . . . He, K. (2017, August 02). Intake of niacin, folate, vitamin B-6, and vitamin B-12 through young adulthood and cognitive function in midlife: The Coronary Artery Risk Development in Young Adults (CARDIA) study | The American Journal of Clinical Nutrition | Oxford Academic. Retrieved from https://academic.oup.com/ajcn/article-abstract/106/4/1032/4652049 Reitz, C. (2012, March 15). Alzheimer's Disease and the amyloid cascade hypothesis: A critical review. Retrieved from https://www.hindawi.com/journals/ijad/2012/369808/abs/ International Journal of Alzheimer's Disease Volume 2012 (2012), Article ID 369808, 11 pages http://dx.doi.org/10.1155/2012/369808 Sealey, R. (2017). PDF [Http://www.searpubl.ca/Review_Niacin_the_Real_Story.pdf]. Basic Health, CA. Thoenes, M., Oguchi, A., Nagamia, S., Vaccari, C. S., Hammoud, R., Umpierrez, G. E., & Khan, B. V. (2007, October 10). The effects of extended‐release niacin on carotid intimal media thickness, endothelial function and inflammatory markers in patients with the metabolic syndrome. Retrieved from http://onlinelibrary.wiley.com/doi/10.1111/j.1742-1241.2007.01597.x/full UHN Staff. (2017, December 07). B vitamins for memory: Niacin benefits for Alzheimer's Disease. Retrieved from https://universityhealthnews.com/daily/memory/b-vitamins-for-memory-niacin-benefits-for-alzheimers-disease/ Williams, J., Plassman, B., Burke, J., Holsinger, T., & Benjamin, S. (2010). Preventing Alzheimer's Disease and cognitive decline. AHRQ Publication No. 10-E005, 193, 1-727. Retrieved from https://www.ahrq.gov/downloads/pub/evidence/pdf/Alzheimers/alzcog.pdf |
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