Alzheimer, feed forward cycle, neocortex, hippocampus and RNA quality


AD is a neurodegenerative disease of complex etiology (2930). The formation of neurofibrillary tangles (NFT), neuropil threads, and senile plaques have been implicated in the onset and development of the disease, but the relative causal weight of these and other factors in sporadic AD continues to be debated (3031). Although initiation and progression of AD may thus be multifactorial, it has been noted that incidence and regional distribution of NFT are most closely associated with the clinical manifestations of the disease (3233). NFT formation is the result of the accumulation of altered components of the neuronal cytoskeleton (34), and it has been suggested that “clogging” of neuronal processes and disruption of long-distance transport may underlie at least some of the cytopathological changes that characterize the disease (19).

We suggest that such cellular changes on one hand and deregulated expression and transport of dendritic RNAs on the other may be causally interrelated in AD. It has recently been speculated that non-protein-coding RNAs may be involved in AD (35), and we now show that expression of dendritic BC200 RNA, which is a translational repressor (35), is differentially regulated in normal aging and in AD. In normal aging, BC200 levels in the neocortex decrease substantially after age 50. Because BC RNAs are prominently located throughout dendrites and at synapses (128), the substantial decline of BC levels may reflect the progressive atrophy of synaptodendritic structures that has previously been observed in normal aging (233639).

In AD, synapse loss and dendritic regression are substantial (40), but these degenerative changes are accompanied by significant dendritic sprouting and remodeling, often in the same neuron (304142). Such reactive developments may be of a compensatory nature, directed at maintaining connectivity and plasticity. In one possible scenario, we therefore suggest that the substantially higher BC200 levels in AD, as compared with those in normal aging, may represent a molecular compensatory effort. If BC200 RNA is needed at the synapse for local translational control, its loss from synaptodendritic domains as the result of dendritic regression and clogging in AD may trigger compensatory mechanisms that result in the increased production of the RNA.

Increased synthesis of key synaptodendritic components may be an appropriate response in situations in which cargoes are not effectively delivered to postsynaptic sites. It may, at least initially or partially, be successful in overcoming moderate dendritic clogging that is caused by altered cytoskeletal components. Over time, however, such response may prove inadequate if further accumulation of cytoskeletal debris creates “roadblocks” that RNAs with dendritic destinations are no longer able to traverse. At this point, relative BC200 levels would begin to decrease in dendrites but increase in somata. In such cases, efforts to compensate would have failed because even increased production could no longer ensure that the RNA reaches its dendritic target sites. Transport deficits have previously been implicated in the progression of AD (1820), and impaired microtubule-dependent transport, coupled with beginning axonal and dendritic blockage, may be an early event in AD that could eventually result in the local generation of amyloid-β peptides and thus in amyloid deposition (17).

Alternative scenarios are possible or even likely. Instead of, or in addition to, being reactive–compensatory to cytoskeletal degeneration, imbalances in the somatodendritic distribution of BC200 RNA could be causative because they may lead to aberrant local translational control. BC200 RNA contains a kink turn motif of the KT-58 subtype that has been implicated in dendritic transport of BC RNAs (943). Because only slight perturbations of the kink turn motif architecture are sufficient to disrupt targeting (9), it is conceivable that single-nucleotide mutations in this region may prevent delivery of the RNA along the dendritic extent. Consequences would be twofold: compensatory elevation of BC200 transcription in an attempt to overcome dendritic delivery block and poor translational control in synaptodendritic domains. Consistent with this model, altered relative BC200 levels become manifest at a very early time point in the course of AD, possibly before clinical signs become detectable (4445).

A gradual worsening of somatodendritic BC200 imbalances may over time set off a self-reinforcing feed–forward cycle. Inadequate translational regulation in dendrites may lead to cytoskeletal overproduction and local dysfunction (16), which in turn would hinder the transport of mRNAs and protein synthetic machinery to postsynaptic target sites. In line with this concept, levels of somatodendritic RC3 mRNA have been shown to be significantly diminished in dendritic regions of AD brains (46). Having been disrupted in this manner, the system would find itself on a slow but accelerating course toward eventual catastrophe, manifesting as synaptic or plasticity failure (17304749). At the same time, increased perikaryal levels of BC200 RNA may inappropriately repress somatic protein synthesis and thus precipitate or exacerbate degenerative changes. We anticipate that future work, directed at the understanding of neuronal RNA transport and local translational control mechanisms, will be able to establish the respective contributions of the causative and reactive–compensatory scenarios.



brain plaques

The study samples come from the Adult Changes in Thought (ACT) study, a longitudinal research effort led by Eric B. Larson, M.D., M.P.H., and Paul K. Crane, M.D., M.P.H., of the Kaiser Permanente Washington Health Research Institute (KPWHRI) (formerly known as Group Health Research Institute) and the University of Washington School of Medicine to collect data on thousands of aging adults, including detailed information on their health histories and cognitive abilities.

“This collaboration with the Allen Institute for Brain Science has allowed us to gain insights never before possible into the relationships between neuropathology, gene expression, RNA quality, and clinical features tracked in the ACT study over more than 20 years,” says Larson, who has led the National Institute of Aging-supported study from its start in 1986 and is Vice President for Research and Health Care Innovation at Kaiser Permanente Washington.


Neural Networks: Sleep and memory – ScienceDirect

by TJ Sejnowski – ‎1995 – ‎Cited by 12 – ‎Related articles

During this generative sleep stage, the strengths of the feedforward synaptic … in the sense that only small changes are made during any one wake–sleep cycle. … sleep, the visual cortex is driven by brain-stem activity and the hippocampus …

Interaction between neocortical and hippocampal networks via slow …

by A SIROTA – ‎2005 – ‎Cited by 139 – ‎Related articles

This might be caused by the removal of tonic and phasic feedforward … pool correlates with the duration of the oscillatory cycle, various brain rhythms can set …

Sleep and Brain Activity – Page 214 – Google Books Result

Marcos G. Frank – 2012 – ‎Medical

So, to the degree that the hippocampal output during ripples originates in … in the prefrontal cortex and spreading through the whole neocortex and brain issue a … a feed forward manner favors the occurrence of another slow oscillation cycle …

Disorders of Brain, Behavior, and Cognition: The Neurocomputational …

J.A. Reggia, ‎E. Ruppin, ‎D.L. Glanzman – 1999 – ‎Medical

… transmission in the piriform cortex, with a much weaker effect on feedforward … in the hippocampusgo much higher than ACh levels in neocortex (Marrosu et al., … rapid changes in modulatory dynamics within each cycle of the theta rhythm.

Microcircuits and their interactions in epilepsy: Is the focus out of focus?

by JT Paz – ‎2015 – ‎Cited by 61 – ‎Related articles

1): 1) feedforward inhibition, in which excitatory inputs from extrinsic brain regions recruit local inhibitory … Feedforward inhibition in neocortex and hippocampus …. This cycle then repeats to propagate seizure activity to the next microcircuit.

Rhythms of the Brain – Page 374 – Google Books Result

Gyorgy Buzsaki – 2006 – ‎Medical

Ahn SM, Freeman WJ (1974) Steady-state and limit cycle activity of mass of … of functionally segregated circuits linking basal ganglia and cortex. … Alger BE, Nicoll RA (1982) Feedforward dendritic inhibition in rat hippocampal pyramidal cells …

Spatially segregated feedforward and feedback neurons support … › nature neuroscience › articles
by FC Leitner – ‎2016 – ‎Cited by 13 – ‎Related articles

May 16, 2016 – The lateral entorhinal cortex (LEC) computes and transfers olfactory … Here we established LEC connectivity to upstream and downstream brain … RE+ neurons provide feedforwardprojections to the hippocampus while …… All animals were housed singly or in pairs and were kept on a 12 h light/dark cycle.

Dynamic Coordination in the Brain: From Neurons to Mind

Christoph von der Malsburg, ‎William A. Phillips, ‎Wolf Singer – 2010 – ‎Medical

From Neurons to Mind Christoph von der Malsburg, William A. Phillips, Wolf Singer … and Transfer at theHippocampus–Entorhinal– Neocortical Interface György Buzsáki … the multisynaptic feedforward loops of the entorhi- nal–hippocampal system, … In each oscillatory cycle, recruitment of principal neurons is temporally …

Handbook of Brain Microcircuits – Page 166 – Google Books Result

Gordon Shepherd, ‎Sten Grillner – 2010 – ‎Medical

(A) Multiple loops of the hippocampal-entorhinal (EC) circuits. … computation in successive layers of the EC-hippocampus (mainly) feedforward loop. … the main direction of information flow, withneocortical– hippocampal transfer taking place … Neurons that discharge within the time period of the gamma cycle (10–30 msec) …

Connie’s comments:
The plaque, clogging , RNA quality and rhythm of the brain circuits are affected by quality of life, whole foods, sleep, stress, and affected by toxins in our environment.
Knowing the effects of the clogging and plaques in our brain from stress, lack of sleep, toxins and inflammation that started in our intestines and environment (pollution, carbon monoxide poisoning, metal toxicities, others) can help us prevent Alzheimer’s. The cure is prevention 20 years before our brain can no longer clean up the plaques and clogs.

For quality supplementation to reset your gene expression to a younger you, visit:

Minimum supplements for seniors: Omega 3, calcium and magnesium with zinc and Vitamin D, Vitamin A, B complex and C.

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9 Health Benefits Of Hemp Oil That You Should Know

9 Health Benefits Of Hemp Oil That You Should Know

by The Z Living Editors

So What Exactly Makes Hemp Oil Healthy?
Hemp Oil Helps Maintain a Hormonal Balance
Hemp Oil Regenerates and Energizes The Skin’s Protective Layer
Hemp Oil Can Help Prevent Varicose Veins
Hemp Oil Helps Prevent Demyelination Of Nervous System
Hemp Oil Can Boost Your Immunity
Hemp Oil Can Be Good For Diabetics
Hemp Oil Helps Lower Cholesterol
Hemp Oil is Great For Vegetarians
Hemp Oil Can Help Prevent Psoriasis

So What Exactly Makes Hemp Oil Healthy?

1 of 10

Hemp seeds are rich in protein, polyunsaturated fatty acids, omega 6, omega 3 and insoluble fiber. They are a good source of tocopherols, or Vitamin E antioxidants. They’re packed with minerals such as potassium, magnesium, iron, zinc, calcium, and phosphorus, plus  microelements like strontium, thorium, arsenic and chromium. High in essential fatty acids, Omega 6 and omega 3, hemp oil can be used to increase immunity, counteract aging skin and improve cardiovascular health. Several studies show that the linoleic acid present in hemp oil can slow down the aging process and fight psoriasis.

Hemp oil or hempseed oil — not to be confused with it’s wilder, headline-grabbing cousin hash oil — is the nutty, flavorful oil that comes from the raw seeds of the hemp plant. While the health benefits of hash oil are questionable, hemp oil’s arent: It’s a documented dietary supplement and beauty aid.

Unfortunately, the widely reported anecdotal claims that hemp oil does much, much more — like miraculously curing cancer and other ailments — are unproven (and likely bogus).

Also on Z Living: These 5 Images Are Scientifically Proven To Relax You

So What Exactly Makes Hemp Oil Healthy? 

Hemp seeds are rich in protein, polyunsaturated fatty acids, omega 6, omega 3 and insoluble fiber. They are a good source of tocopherols, or Vitamin E antioxidants. They’re packed with minerals such as potassium, magnesium, iron, zinc, calcium, and phosphorus, plus  microelements like strontium, thorium, arsenic and chromium.

High in essential fatty acids, Omega 6 and omega 3, hemp oil can be used to increase immunity, counteract aging skin and improve cardiovascular health. Several studies show that the linoleic acid present in hemp oil can slow down the aging process and fight psoriasis.

Also on Z Living10 Incredible Benefits of Couscous

Here Are Hemp Oil’s Most Significant Health Benefits:

  1. Hemp Oil Helps Maintain a Hormonal Balance: Hemp is the only edible seed that contains gamma-linolenic acid, which is eventually converted to the protective hormone prostaglandin PGE1 that regulates the hormonal balance and supports menopausal health.
  2. Hemp Oil Regenerates and Energizes The Skin’s Protective Layer: Due to its high content of omega 3 and omega 6 fatty acids, hemp oil has a composition similar to skin lipids, which makes it an excellent natural emollient and moisturizer. It is especially useful for dry, tired or dehydrated skin and nails. It increases the skin elasticity and water retention capacity in tissues. Pure hemp oil can be used to treat dry hair and is often included in hair conditioners.
  3. Hemp Oil is Great For Vegetarians: Getting the right balance of omega-3 and omega-6 fatty acids can be tricky for vegetarians and vegans. Hemp oil has the optimal ratio of these acids.
  4. Hemp Oil Helps Lower Cholesterol: The only vegetable oil to contain omega-3 and omega-6 fatty acids (3:1), hemp oil can help lower cholesterol levels by accelerating metabolic processes. With a faster metabolism, fats burn at a quicker rate and are not deposited on the artery walls.
  5. Hemp Oil Can Be Good For Diabetics: Due to its low carbohydrate and sugar content, hemp oil is can be a great food additive for diabetics. The nutrients present in it can help moderate blood sugar levels.
  6. Hemp Oil Can Help Prevent Psoriasis: Psoriasis is caused by a deficiency of omega-6 fatty acids in the body. The fatty acids present in hemp oil help improve skin oxygenation and hydration.
  7. Hemp Oil Can Boost Your Immunity: Omega-3 and omega-6 fatty acids also improve immunity and regulate intestinal flora, thus building a natural barrier against microbes and increasing the resilience of the body.
  8. Hemp Oil Helps Prevent Demyelination Of Nervous System: Essential fatty acids are necessary for a healthy cell membrane structure. They also prevent the demyelination, the destruction of the myelin sheath (a membrane that protects the nerve cells).
  9. Hemp Oil Can Help Prevent Varicose Veins: Like other compounds high in omega-3s, hemp oil can thin your blood, reducing blood clots and varicose veins.

Also on Z Living: 3 Big Ways Our New Show ‘Conquered’ Will Change Your Life

Precautions To Keep In Mind When Trying Hemp Oil For The First Time

Though it has a number of health benefits, hemp oil should be avoided by prostate cancer patients or people who take blood thinners. Here are a few precautions you should keep in mind before using it:

  • It’s an Anticoagulant: Hemp oil can have an anti-clotting effect on the blood. People who suffer from heart diseases and take blood thinners should avoid it (or at least check with a doctor before use!)
  • It Can Increase Prostate Cancer Risk: Hemp oil has been shown to creates the best conditions for the cells to regenerate, which could promote the growth of tumors, particularly prostate cancer cells. While more research is needed, medical professionals advise that you avoid consuming hemp oil if you are at an increased risk of prostate cancer.
  • In High Doses, It Could Cause Diarrhea or Cramps: Large doses of hemp oil can cause nausea, diarrhea and/or abdominal cramps. For this reason, hemp oil should be kept out of the reach of children.
  • It Shouldn’t Be Heated: High temperatures can denature the unsaturated fats of hemp oil and turn them into saturated fats.

Dogfish shark steroid could help to prevent the build up parkinson’s

Summary: A synthesised steroid similar to that naturally made by the dogfish shark could help to prevent the build up of alpha synuclein.

Source: GUMC.

A synthesized steroid mirroring one naturally made by the dogfish shark prevents the buildup of a lethal protein implicated in some neurodegenerative diseases, reports an international research team studying an animal model of Parkinson’s disease. The clustering of this protein, alpha-synuclein (α-synuclein), is the hallmark of Parkinson’s and dementia with Lewy bodies, suggesting a new potential compound for therapeutic research.

The finding, published online in Proceedings of the National Academy of Sciences, also demonstrated that the synthesized steroid, called squalamine, reduced the toxicity of α-synuclein clumps that already existed.

The pre-clinical study results show that squalamine prevents and eliminates α-synuclein build up inside neurons by unsticking the protein from the inner wall of nerve cells, where it clings and builds up into toxic clumps, researchers say.

The animal model used for this study, C. elegans, is a nematode worm genetically engineered to produce human α-synuclein in its muscles. As these worms age, α-synuclein builds up within their muscle cells causing cell damage and paralysis.

“We could literally see that squalamine, given orally to the worms, did not allow α-synuclein to cluster, and prevented muscular paralysis inside the worms,” says the study’s co-senior author, Michael Zasloff, MD, PhD, professor of surgery and pediatrics at Georgetown University School of Medicine and scientific director of the MedStar Georgetown Transplant Institute.

The study’s lead author, graduate student Michele Perni, and other co-senior authors, Michele Vendruscolo, PhD and Christopher M. Dobson, DPhil, ScD, are from Cambridge University. An additional co-senior author, Adriaan Bax, PhD, is from National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health (NIH) in Bethesda, Maryland. Scientists from the Netherlands, Italy and Spain also contributed to this research.

Zasloff, an expert in innate immune systems, has been studying squalamine for more than 20 years. He discovered it in dogfish sharks in 1993 and synthesized it in 1995 (in a process that does not involve use of any natural shark tissue). His research, as well as that by other scientists, has established antiviral and anticancer properties of the compound. This is the first study to show it has neurological benefits in in vivo models of Parkinson’s.

In Parkinson’s disease, α-synuclein, a normal protein present within the nervous system, forms toxic clumps that damage and ultimately destroy the neurons in which they form. Considerable research has been directed at discovering compounds that prevent the formation of these masses, thereby representing potential therapeutics for Parkinson’s disease.

Image shows a Spiny Dogfish shark.

In this study, the researchers demonstrated in a series of in vitro experiments that squalamine, a positively charged molecule with a high affinity for negatively charged membranes, could literally “kick off” α-synuclein from negatively charged membranes, where the protein binds, preventing the formation of the toxic clumps.

The research team also showed that squalamine could protect healthy human neuronal cells from being damaged by exposure to pre-formed toxic masses of α-synuclein, by preventing them from adhering to the outer membrane of the neuronal cells.

The researchers then extended these studies to a living system, C. elegans, a well-studied model of Parkinson’s disease. “Orally administered squalamine prevented the formation of toxic α-synuclein clumps in this complex animal, and rescued the animal from loss of mobility,” Zasloff explains. “This experiment taught us that the basic mechanism demonstrated in vitro achieved the anticipated outcome in an animal.”


The study’s co-senior author, Professor Christopher Dobson, DPhil, Master of St John’s College, University of Cambridge says, “Squalamine gives us a first generation compound, which we believe that we can incrementally improve through further studies of the underlying mechanism by which it affects the aggregation of alpha-synuclein.”

Zasloff says a clinical trial with squalamine in Parkinson’s disease is being planned. “Squalamine could be especially suited to work in the gut with the goal of treating the gastrointestinal symptoms of Parkinson’s,” he adds.

Zasloff is the inventor on a patent application that has been filed related to the technology described in this paper. The other authors report having no personal financial interests related to the study.

Additional authors include Celine Galvagnion, Georg Meisl, Martin B. D. Müller, Pavan K. Challa, Patrick Flagmeier, Samuel I. A. Cohen, Pietro Sormanni, Gabriella T. Heller, Francesco A. Aprile, Tuomas P. J. Knowles, Michele Vendruscolo, Serene W. Chen, Ryan Limbocker and Julius Kirkegaard from the University of Cambridge, England; Alexander S. Maltsev, from NIDDK; Ellen A. Nollen, from the European Research Institute for the Biology of Aging, Groningen, The Netherlands; Roberta Cascella, Cristina Cecchi, and Fabrizio Chiti, from the University of Florence; and Nunilo Cremades, from the University of Zaragoza, Spain.

Funding: The study was funded by the NIH Intramural Research Program, the Boehringer Ingelheim Fonds, the European Research Council (ERC), and the Centre for Misfolding Diseases at Cambridge.

Source: Karen Teber – GUMC
Image Source: image is credited to Doug Costa, NOAA/SBNMS.
Original Research: Full open access research for “Squalamine as a broad-spectrum systemic antiviral agent with therapeutic potential” by Michael Zasloff, A. Paige Adams, Bernard Beckerman, Ann Campbell, Ziying Han, Erik Luijten, Isaura Meza, Justin Julander, Abhijit Mishra, Wei Qu, John M. Taylor, Scott C. Weaver, and Gerard C. L. Wong in PNAS. Published online January 16 2017 doi:10.1073/pnas.1108558108

GUMC “Steroid in Dogfish Shark Attacks Parkinson’s Toxin: Animal Study.” NeuroscienceNews. NeuroscienceNews, 16 January 2017.


Squalamine as a broad-spectrum systemic antiviral agent with therapeutic potential

Antiviral compounds that increase the resistance of host tissues represent an attractive class of therapeutic. Here, we show that squalamine, a compound previously isolated from the tissues of the dogfish shark (Squalus acanthias) and the sea lamprey (Petromyzon marinus), exhibits broad-spectrum antiviral activity against human pathogens, which were studied in vitro as well as in vivo. Both RNA- and DNA-enveloped viruses are shown to be susceptible. The proposed mechanism involves the capacity of squalamine, a cationic amphipathic sterol, to neutralize the negative electrostatic surface charge of intracellular membranes in a way that renders the cell less effective in supporting viral replication. Because squalamine can be readily synthesized and has a known safety profile in man, we believe its potential as a broad-spectrum human antiviral agent should be explored.

“Squalamine as a broad-spectrum systemic antiviral agent with therapeutic potential” by Michael Zasloff, A. Paige Adams, Bernard Beckerman, Ann Campbell, Ziying Han, Erik Luijten, Isaura Meza, Justin Julander, Abhijit Mishra, Wei Qu, John M. Taylor, Scott C. Weaver, and Gerard C. L. Wong in PNAS. Published online January 16 2017 doi:10.1073/pnas.1108558108

Japanese, Germans and American Omega 3 levels

omega 3.JPG

  • Japanese are almost at 9. Not bad!
  • Germans are at 6. So-so.
  • Americans are, ahem, at 4.

Benefit of Omega 3

  • Omega-3s are important for heart, brain, and joint health.
  • Most Americans have low levels of omega-3s in their blood.
  • Low levels of omega-3s are related to increased risk for fatal heart attack, depression, and possibly dementia.
  • Blood levels of omega-3s can be improved by simple dietary changes.
  • The only way to know your blood level of omega-3s is by measuring it, with the Omega-3 Index.

Email to be tested for Omega 3 in one drop of your blood (test costs $55 to $100 per test).

Know your fats


Trans Fat, the bad fat

  • Trans fats in your blood come from trans fats in food.
  • Most Americans have high levels of trans fats in their blood.
  • High levels of trans fats are related to increased risk for heart disease.
  • Blood levels of trans fats can be reduced by simple dietary changes.

Signs of Lupus in women

Systemic lupus erythematosus (SLE), also known simply as lupus, is an autoimmune disease in which the body’s immune system mistakenly attacks healthy tissue in many parts of the body.[1] Symptoms vary between people and may be mild to severe. Common symptoms include painful and swollen joints, fever, chest pain, hair loss, mouth ulcers, swollen lymph nodes, feeling tired, and a red rash which is most commonly on the face. Often there are periods of illness, called flares, and periods of remission when there are few symptoms.[1]

The cause is not entirely clear.[1] It is believed to involve hormonal, environmental, and genetic factors.[2] Among identical twins, if one is affected there is a 24% chance the other one will be as well.[1] Female sex hormones, sunlight, smoking, vitamin D deficiency, and certain infections, are also believed to increase the risk.[2] The mechanism involves an immune response by autoantibodies against a person’s own tissues. These are most commonly anti-nuclear antibodies and they result in inflammation. Diagnosis can be difficult and is based on a combination of symptoms and laboratory tests. There are a number of other kinds of lupus erythematosus including discoid lupus erythematosus, neonatal lupus, and subacute cutaneous lupus erythematosus


The global rates of SLE are approximately 20-70 per 100,000 people. In females, the rate is highest between 45-64 year of age. The lowest overall rate exists in Iceland and Japan. The highest rates exist in US and France. However, there is no sufficient evidence to conclude that SLE is less common in some countries compared to others, since there is significant environmental variability in these countries. For example, different countries receive different levels of sunlight, and exposure to UV rays affects dermatological symptoms of SLE. Certain studies hypothesize that a genetic connection exists between race and lupus which affects disease prevalence. If this is true, the racial composition of countries affects disease, and will cause the incidence in a country to change as the racial makeup changes. In order to understand if this is true, countries with largely homogenous and racially stable populations should be studied to better understand incidence.[5] Rates of disease in the developing world are unclear.[6]

The rate of SLE varies between countries, ethnicity, sex, and changes over time.[87] In the United States, one estimate of the rate of SLE is 53 per 100,000;[87] other estimates range from 322,000 to over 1 million.[88] In Northern Europe the rate is about 40 per 100,000 people.[89] SLE occurs more frequently and with greater severity among those of non-European descent.[88] That rate has been found to be as high as 159 per 100,000 among those of Afro-Caribbean descent.[87] Childhood-onset systemic lupus erythematosus generally presents between the ages of 3 and 15 and is four time more common in girls.[90]

While the onset and persistence of SLE can show disparities between genders, socioeconomic status also plays a major role. Women with SLE and of lower socioeconomic status have been shown to have higher depression scores, higher body mass index, and more restricted access to medical care than women of higher socioeconomic statuses with the illness. People with SLE had more self-reported anxiety and depression scores if they were from a lower socioeconomic status.[91]


There are assertions that race affects the rate of SLE. However, a 2010 review of studies which correlate race and SLE identified several sources of systematic and methodological error, indicating that the connection between race and SLE may be spurious.[92] For example, studies show that social support is a modulating factor which buffers against SLE-related damage and maintains physiological functionality.[92] Studies have not been conducted to determine whether people of different racial backgrounds receive differing levels of social support.[92] If there is a difference, this could act as a confounding variable in studies correlating race and SLE. Another caveat to note when examining studies about SLE is that symptoms are often self-reported. This process introduces additional sources of methodological error. Studies have shown that self-reported data is affected by more than just the patients experience with the disease- social support, the level of helplessness, and abnormal illness-related behaviors also factor into a self-assessment. Additionally, other factors like the degree of social support which a person receives, socioeconomic status, health insurance, and access to care can contribute to an individual’s disease progression.[92][93] It is important to note that racial differences in lupus progression have not been found in studies that control for the socioeconomic status [SES] of participants.[92][94] Studies that control for the SES of its participants have found that non-white people have more abrupt disease onset compared to white people and that their disease progresses more quickly. Non-white patients often report more hematological, serosal, neurological, and renal symptoms. However, the severity of symptoms and mortality are both similar in white and non-white patients. Studies that report different rates of disease progression in late-stage SLE are most likely reflecting differences in socioeconomic status and the corresponding access to care.[92] The people who receive medical care often have accrued less disease-related damage and are less likely to be below the poverty line.[94] Additional studies have found that education, marital status, occupation, and income create a social context which contributes to disease progression.[92]


SLE, like many autoimmune diseases, affects females more frequently than males, at a rate of about 9 to 1.[3][87] The X chromosome carries immunological related genes, which can mutate and contribute to the onset of SLE. The Y chromosome has no identified mutations associated with autoimmune disease.[95]

Hormonal mechanisms could explain the increased incidence of SLE in females. The onset of SLE could be attributed to the elevated hydroxylation of estrogen and the abnormally decreased levels of androgens in females. In addition, differences in GnRH signalling have also shown to contribute to the onset of SLE. While females are more likely to relapse than males, the intensity of these relapses is the same for both sexes.[96]

In addition to hormonal mechanisms, specific genetic influences found on the X chromosome may also contribute to the development of SLE. Studies indicate that the X chromosome can determine the levels of sex hormones. A study has shown an association between Klinefelter syndrome and SLE. XXY males with SLE have an abnormal X-Y translocation resulting in the partial triplication of the PAR1 gene region.

Keeping Your Immune System Healthy

How do you keep the immune system active and healthy? All the books say essentially the same thing— simply by living well. And “living well” involves common sense practices such as eating a healthful diet, getting enough sleep, exercising, drinking alcohol only in moderation, and avoiding stress. A few additional tips for keeping the immune system healthy include:

  • Avoid or prevent exposure to environmental toxins such as mercury, poisons and heavy metals.
  • Avoid taking unnecessary drugs.
  • Understand that diet can influence your immune system, and choose your foods wisely.
  • Have sex. Sexual activity has been found to be good for the immune system because it activates the hormones that are regulated by the act of having sex and helps maintain a healthy hormone balance.


Diet for the elderly

A personalised nutrition approach
Micronutrients such as zinc, copper and selenium play a pivotal role in a range of physiological functions and maintain immune and antioxidant systems (Eugenio Mocchegiani et al.). The complex interactions between micronutrients and genes could help in understanding how best to use nutrients as supplements in clinical practice. Further genetic and nutritional studies are required to clearly define the impact of these micronutrients.
Targeting the human gut microbiome (Sebastiano Collino et al.) is an emerging field of personalised nutrition. This approach could help to identify key molecular mechanisms affected by diet and inflammaging, and lead to basic profiles of health and diagnostic tools to address conditions such as inflammatory bowel disease.
Three papers cover the interaction between diet and the gut microbiota (Candela et al.), the effect of an elderly tailored diet on cognitive decline and brain and gut connections, including the liver and pancreas (Caracciolo et al.). Nutritional interventions such as low calorie intake with nutrient supplementation can impact an individual’s cell epigenetic profile e.g. DNA methylation, microRNA and organs (Bacalini et al.). Better knowledge of gene interactions with nutrients and the environment may lead to earlier interventions of malnutrition in people (Yves Boirie et al.). And more genomic information may identify impacts of general health recommendation policies in at-risk, elderly sub-populations.
The effect of diet on immunosenescence, which is the functional decline of the immune system (Maijo´ et al.), and changes that happen in ageing fat tissue (Zamboni et al.) are both assumed to be major sources of inflammation. Nutritional interventions have shown some promising results in targeting some impairments of an ageing immune system; combining interventions with a whole diet approach could be more beneficial.
It is commonly known that physical exercise can benefit health and age-related decline. In one study (van de Rest et al.), resistance-type exercises, using a number of body techniques and workout machines, with and without protein supplementation, was undertaken to see the effect on cognitive functions in frail and pre-frail elderly people. After 24 weeks of training a beneficial improvement was noted in participants’ information processing speed, attention and working memory.

food pyramid

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