Cera-Q – The Anti-Aging Supplement From a Silkworm
Getting old sucks. From the physical standpoint, our metabolism slows down, muscle gain and fat loss become more difficult, and joints stiffen. From the cognition standpoint, our forgetfulness increases, it becomes more difficult to learn new tasks, and our brain physically shrinks in volume.
In the early 2000s, a group of researchers from South Korea began exploring all-natural compounds that could fight brain aging and discovered one of the most unlikely heroes – the silkworm. Specifically, the cocoon of the species Bombyx mori.
As we age, harmful protein called beta-amyloid plaque builds up in the brain. This plaque degrades neuron membrane receptors, blocks cell-to-cell signaling, and increase whole-body inflammation.  Researchers currently believe the buildup of beta-amyloid plaques is the primary cause of Alzheimer’s, the most common neurodegenerative disease on the planet.
Cera-Q is a protein hydrolysate extracted from fibroin, the major protein in silkworm cocoons.  Traditional Korean medicine has prescribed silkworm fibroin for centuries to improve health and longevity. This protein’s high glycine and alanine content (~75% of the total amino acid composition), paired with a unique molecular structure, offers the unique advantage of binding to and preventing the buildup of amyloid plaque in the human brain. 
In addition to fighting against beta-amyloid plaque buildup, Cera-Q can also increase glucose uptake to the brain which provides energy and support during both simple and complex cognitive tasks.  Multiple studies on humans, animals, and cells verify Cera-Q potency and efficacy as an anti-aging compound for the brain.
The process for isolating Cera-Q is somewhat complex. Researchers place the silkworm cocoon in a mixture containing water and proprietary enzymes to isolate the fibroin protein found into a combination of short chains of amino acids called peptides.  After isolating the protein in hydrolysate form, the mixture is dried to eliminate the water so that only the protein remains.
The result is Cera-Q powder. Cera-Q is a water-soluble tan to yellowish-tan powder with greater than 65% protein and less than 10% moisture by weight, a semi-sweet taste like the amino acid L-glycine, and a shelf life of up to two years. 
To fight aging and cognitive decline the manufacturers of Cera-Q recommend a dosage of 200mg to 400mg per day divided across two to three servings.  One study found minor benefit with a dosage as low as 10mg per day but most research uses a daily 200mg to 400mg dosage. The dosage varies slightly based on the desired application of Cera-Q, characteristics of the end user, and other ingredients that may be included in a supplement containing Cera-Q.
Higher doses offer a greater benefit when consumed for a short period but also carry a higher cost. A lower dose is more cost-efficient and beneficial when consumed chronically for a longer period but may not offer the immediate benefits seen with higher doses.
You can purchase Cera-Q Silk Protein Hydrolysate as a single ingredient supplement or as a part of a multi-ingredient blend in gummy chews, beverage, shot, powder, tablet, and capsule forms.  There is a form of Cera-Q for your regardless of how you prefer to take your supplements.
Cera-Q also works synergistically with caffeine when consumed together in a one to one ratio. 200 to 400mg of each compound can improve brain circulation, deliver more glucose to the brain, release more fatty acids, and create a blood pressure neutral environment. Cera-Q decreases blood pressure whereas caffeine increases blood pressure.
Studies on animals and human cells confirm silk protein hydrolysate’s ability to fight against harmful beta-amyloid plaques that build up in the brain as we age. Cera-Q also reduces the amount of dead tissue resulting after ischemia, an event in which a vital organ (usually the heart) or body part receives an inadequate blood supply.
Researchers injected beta-amyloid protein in the hippocampal region of rat brains and then provided 5 to 10mg per kilogram of bodyweight oral doses of Cera-Q to rats for two continuous weeks. The beta-amyloid protein reduced acetylcholine levels in the brain by 45%. Just 5 to 10mg of Cera-Q per kilogram of bodyweight restored acetylcholine levels to between 78 and 80% of the levels found in the control population. 
Low levels of acetylcholine significantly impair learning, memory, and cognitive function. A study on human cells found that administering Cera-Q two hours prior to administering beta-amyloid protein normalized cell appearance and prevented 85% of cell death compared to the control group.  Beta-amyloid protein buildup in the brain paired with high rates of cell death expedites the aging process and neurodegeneration.
Cera-Q exhibits antioxidant properties through its ability to protect against reactive oxygen species. High levels of reactive oxygen species in the body hamper our immune system and increase inflammation. Reactive oxygen species levels were 65% lower in cells receiving Cera-Q after receiving beta-amyloid proteins and just 15% higher than the control cells receiving no beta-amyloid proteins. 
As we age we also experience an increased likelihood of insufficient blood supply to vital organs. Researchers blocked the middle carotid artery of rats and then provided them with a 10mg per kilogram dose of Cera-Q daily or placebo for seven days.
Rats receiving Cera-Q had a smaller area of dead tissue around the area damaged insufficient blood supply, experienced a smaller loss of neurons, and improved memory compared to the control group.  Silk protein hydrolysates in the form of Cera-Q may become a staple compound in fighting against heart attacks and Alzheimer’s.
A sharp mind and lucid memory is critical for fighting the aging process. The studies on Cera-Q consumption in humans found that it benefits the memory and learning capabilities of children, adults, and seniors.
In 2004, 53 healthy Korean females and 13 healthy Korean males with an average age of 42 consumed either 0mg, 200mg, or 400mg of Cera-Q daily for three weeks. These individuals then completed Digit Symbol Test portion the Korean-Wechsler Adult Intelligence Scale. The Digit Symbol Test is a variation of number memorization used to measure brain damage, dementia, age, and depression. 
Individuals consuming placebo did not show improvement over baseline but those consuming 200mg and 400mg of Cera-Q increased their scores by 11.3% and 22.2%, respectively.  These results are staggering after just three weeks of supplementation.
A larger study of 99 healthy Korean adults asked individuals to consume 0mg placebo, 200mg, or 400mg of Cera-Q daily for three weeks and perform the Rey-Kim Memory Test.  This test measures both auditory and visual memory.  The placebo group experienced no improvements but both Cera-Q groups experienced significant improvements in memory maintenance as measured by word recall in a dose dependent manner. 
This means that the 400mg group had superior improvements in word recall compared to the 200mg group. The 200mg and 400mg groups also improved memory recall efficiency by 90% and 60%, respectively, compared to their intra-group baseline.  The baseline memory recall efficiency was higher for those in the 400mg group compared to the 200mg group.
This 99-person study also examined everyone’s memory quotient (MQ) and found the pre-study average to be 105.  Memory quotient assesses memory for content, location, and sequence as measured by questions related to short-term recall and recognition of both meaningful and abstract material.  A low memory quotient indicates diminished or impaired memory and logic.
At the end of the study researchers found that those in the placebo group increased their memory quotient by 3% but those in the 200mg and 400mg Cera-Q groups increased their memory quotient by a staggering 12% and 21%, respectively.  Keeping a sharp memory is critical for fighting the aging process and silk protein hydrolysate may be one of the most potent substance to help you do so.
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Polyphenols have been shown to exhibit neuroprotective effects suppress neuroinflammation and activate antioxidant mechanisms.
A polyphenol found in pomegranate fruit, punicalagin, inhibits neuroinflammation in LPS-activated rat primary microglia by suppressing the production of pro-inflammatory cytokines (TNF- and IL-6), and PGE2 after 24 h of stimulation with LPS.
Punicalagin, which is a polyphenol – a form of chemical compound found in pomegranate fruit, can inhibit inflammation in specialised brain cells known as microglia. This inflammation leads to the destruction of more and more brain cells, making the condition of Alzheimer’s sufferers progressively worse . Recent results suggest that punicalagin inhibits neuroinflammation in microglia through interference with NF-[kappa]B signalling.
It is recommended to consume juice products that are 100 per cent pomegranate, meaning that approximately 3.4 per cent will be punicalagin. Unfortunately, most of the anti-oxidant compounds are found in the outer skin of the pomegranate, not in the soft part of the fruit. Pomegranate may be useful in neuroinflammatory conditions other than Alzheimer’s disease, including cancer and Parkinson’s disease.
Bottom Line: EAT YOU pomegranates! Punicalagin is good for your brain. The juice is the best was to get the most of the phytonutrient. It’s role in reducing the risk of Alzheimer’s disease and other inflammatory conditions is still being evaluated, but seems very promising.
Below is Nonsense relating to neuroinflammation, studies involving Punicalagin, and cytokines in the CNS:
Cytokines are polypeptides (proteins) that cause inflammation, immune activation, cellular differentiation, and death. They include interferons (INF) , tumor necrosis factor (TNF) , interleukins(IL) , chemokines, and growth factors. None of these are present to any degree in healthy tissues, but rather are induced by cell damage and tissue injury.
In the CNS, Tumor necrosis factor alpha (TNFa), Interleukin-1 (IL-1), and Transforming Growth Factor Beta (TGFb) are primarily the main cytokines. Each of these cytokines binds a specific receptor, which activates a process or signaling pathway, which include the NfkB and MAPK (mitogen activated protein kinase) pathways.
In the CNS, other cytokines include:
Chemokines (fractalkine, IL-8, RANTES)
Neuropoietic cytokines (IL-6, IL-11)
In a very basic categorization, the pro-inflammatory cytokines are : IL-1, TNF-a, IL-6, and the anti-inflammatory cytokines are IL-1ra (IL-1 receptor antagonist), IL-10, and TGFb
It has been noted that TNFa and IL-1 increase in the brain prior to neuronal death, and there are increased cytokines in stroke. The presence of IL-6 and TNFa are found to be increased in areas of tissue injury and in tissues in which there were poor clinical outcomes.
Some cytokines are synergistic – i.e. IL1 and TNFa or INFg (gamma) cause neurotoxicity when they are around together. TNFa may have a dose-dependent neurotoxicity.
IL-1ra inhibits brain damage caused by injury or excitotoxins.
If you inhibit IL-1ra, it has been found that ischemic damage occurs more frequently, hence IL-1ra is protective in the brain. If you block it, then you lose protection.
TGFB2 receptor (which binds protective TGFB), will induce damage in the brain by removing the protective TGFB, but having too much TGFb causes autoimmune encephalitis. Thus too much of a good thing can cause problems as well!
SO again :
IL-1 = neurodegenerative
IL-10 = protective against injury
TNFa/IL-6 cause damage, but sometimes inhibit damage. It’s not always just they cytokines presence but WHEN they are present that counts. Il-1 and TNFa protect neurons if they are present BEFORE an injury, but if delivered at the time of injury, they cause destruction.
Different cells in the brain secrete cytokines. Glia, endothelial cells (lining of blood vessels), microglia, and neurons express TNFa, which in turn induces IL-10 that feeds back to decrease TNFa production (negative feedback). There is a TNF alpha binding protein that influences and decreases TNFa and also fractalkins that cause microglia to secrete less TNFa as well. All of these create feedbacks to limit cytokine production in complicated ways.
When damage occurs, the microglia (structural cells in the brain) first produce IL-1b(beta). The damage to cells causes extracelular ATP to be released and that activates P2X7 receptors that cause decreased intracellular potassium. This results in caspase 1 activation that causes the production of IL-1B, which in turn KILLS microglia and macrophages in the brain.
Also, during injury, TNFa release causes TGFb/IL6 expression.
Injury causes IL-1 to induce TNFa, IL-6, TGFb expression as well!
Infection and inflammation in the brain or periphery cause increased CNS cytokines and further inflammation. Hence peripheral inflammation affects CNS inflammation as well.
Excitotoxic amino acids also regulate cytokines after CNS injury as below:
Postsynaptic Density Protein 95 binds NMDA receptor subunit NR2 and Kainate recptor GLUR6 – which then phosphorylates C-JUn-N terminal kinase (JNK) and activates JUN. JUN promotes IL-1, IL-6, TNFa, INFa/g production.
Of note Cannabomids INHIBIT TNFa and IL-1 release from glial cells and are anti-inflammatory.
Neurons depend on glial cells for survival. Glial cells (astrocytes) produce neurotropins and growth factors (nerve growth factor (NGF), BDNF, GDNF)
Cytokines affect blood flow in the CNS as well indirectly. IL-1 induces neovasculariztion. IL-1 and TNFa damage the blood brain barrier and allow migration of molecules in and out of the CNS. They also cause NO (Nitric oxide) to be released, which is neurotoxic. They also upregulate adhesion molecules for leukocytes, that then enter the brain. What follows in vasogenic edema (swelling).
IL-1, IL-6, and TNFa also mediate fevers, endocrine reactions, and cardiovascular changes. This causes increased neuronal loss by alterations in blood flow and inflammation.
The COX-2 enzyme pathway and subsequent generation of prostaglandins play a significant role in neuroinflammation. mPGES-1 is the terminal enzyme for the biosynthesis of PGE2 (prostoglandin) during inflammation, and is functionally coupled with COX-2. This enzyme is markedly induced by pro-inflammatory stimuli and is down-regulated by antiinflammatory glucocorticoids – mPGES-1 inhibitors produced inhibition of PGE2 production
The transcription factor NF-B plays a crucial role in neuro-inflammation.
In resting cells, NF-B is sequestered in the cytoplasm by the inhibitory IB protein. When activated by a variety of stimuli that includes LPS (lipopolysacharride), IB is phosphorylated by IKK. Phosphorylated IB then undergoes ubiquitinisation and degradation . Dissociation and degradation of IB activates the translocation of NF-B subunit from the cytosol to the nucleus. The translocated subunit thereafter facilitates the transcription of several pro-inflammatory genes, including those encoding pro-inflammatory cytokines, and COX-2. Furthermore, microglial NF-B activation has been linked to brain damage
Punicalagin significantly inhibited LPS-induced NF-B signalling in microglia by suppressing the phosphorylation of IKK, IB and nuclear p65
Punicalagin produced a modest suppressive action on the phosphorylation of p38 and JNK MAPKs following LPS activation
Treatment with LPS in primary astrocytes triggered the synthesis of inflammatory cytokines, through MAPKs signalling pathways. Of particular interest is the role of p38, which has been shown to be a critical mediator of LPS-induced inflammation .
It appears that the effects of punicalagin on neuroinflammation are mediated mainly through targeting NF-B signalling, while MAPKmediated actions are minimal. Studies have shown that the TLR-4-mediated TRAF- 6/IKK/NF-B pathway has been well established as a signalling pathway responsible for inflammatory responses.
In addition to NF-B activation, TLR-4 can also initiate MAPK signalling
Punicalagin inhibited TRAF-6 protein expression, suggesting that this compound may inhibit the IKK/IB/NF-B signalling pathway, as well as p38 and JNK MAPK via selective inhibition of TRAF-6
Treatment with LPS in primary astrocytes triggered the synthesis of inflammatory cytokines, through MAPKs signalling pathways.
The p38 MAPK inhibitors for the treatment of inflammatory diseases and cancer <<– The p38 MAPK signaling cascade is involved in various biological responses other than inflammation such as cell proliferation, differentiation, apoptosis and invasion. The p38 MAPK, originally referred as cytokine-suppressive anti-inflammatory drug binding protein (CSBP). p38 MAPK is activated by pro-inflammatory cytokines such as interleukins and TNF-α. Stimulation of receptors that initiate this cascade include GPCR, cytokine receptors, Toll-like receptors, growth factor receptors, and receptors associated with environmental stress such as heat shock, radiation and ultraviolet light. p38 MAPK is activated by upstream MAPK kinases (MKK) p38 MAPK pathway plays a central role in the expression and activity of pro-inflammatory cytokines such as TNF-α, IL-1, IL-2, IL-6, IL-7, and IL-8 and plays a regulatory role in cell proliferation and differentiation in the immune system. It also regulates the expression of several MMPs involved in inflammation such as MMP-2, MMP-9, and MMP-13.
There is involvement of p38 MAPK in cancer cell invasion. Of note, p38α and p38β were found to play important roles in cell differentiation and invasion of several different cancer cells such as breast cancer, squamous carcinoma cell, colon cancer, and ovarian cancer
Common pathways of neuronal cell death have been identified in response to diverse insults, such as ischaemia, trauma or excitotoxicity. These include early disruption of ion homeostasis, excessive neuronal activation, seizures and spreading depression, massive release and impaired uptake of neurotransmitters such as glutamate, intracellular entry of Ca2+, and release of nitric oxide and free radicals. More recently, further factors have been identified, including activation of genes that initiate or execute apoptosis, and the influence of glial and endothelial cells, extracellular matrix and invading immune cells. There is evidence that specific cytokines can act at most, if not all, of these steps, and probably have multiple actions on several cells or systems involved in neurodegeneration.
Increased expression of p38 MAPK and extracellular-signal-regulated kinase (ERK) has been found in ischaemic brain tissue after MCAo. Selective inhibitors of these pathways markedly reduce the ischemic injury in rodents. TNFR1 and TNFR2 (Tumor necrosis factor receptors) belong to the low-affinity neurotrophin receptor gene superfamily. TNFα elicits its biological effects on multiple cell types in the CNS through these receptors.
TGFβ- mediated signalling is also regulated through crosstalk with other signal transduction pathways, including MAPK.
So, IL-1ra, or a small molecule antagonist of IL-1 receptors, might be beneficial in acute neurodegenerative conditions. Studies are currently evaluating this.
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Chao, C. C., Hu, S., Ehrlich, L. & Peterson, P. K. Interleukin-1 and tumor necrosis factor-α synergistically mediate neurotoxicity: involvement of nitric oxide and of N-methylD-aspartate receptors. Brain. Behav. Immun. 9, 355–365 (1995). An early study showing interactions between cytokines to influence neuronal death in vitro, using human fetal brain cell cultures composed of neurons and glia.
Nawashiro, H., Martin, D. & Hallenbeck, J. M. Inhibition of tumor necrosis factor and amelioration of brain infarction in mice. J. Cereb. Blood Flow Metab. 17, 229–232 (1996). An early study indicating that endogenous TNFα mediates ischaemic brain damage in vivo. TNFbinding protein — a naturally occurring inhibitor of TNF — reduced damage caused by focal cerebral ischaemia in mice.
Scherbel, U. et al. Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury. Proc. Natl Acad. Sci. USA 96, 8721–8726 (1999). This study might provide an explanation for seemingly conflicting reports indicating that endogenous TNFα is either neurotoxic (based largely on acute interventions) or neuroprotective (based largely on stadies on genetically modified animals). It reports that functional outcomes in TNFα-null mice were improved early after brain injury compared with wild type mice, but TNFα-null mice showed permanent deficits and reduced recovery.
Ferrari, D., Chiozzi, P., Falzoni, S., Hanau, S. & Di Virgilio, F. Purinergic modulation of interleukin-1β release from microglial cells stimulated with bacterial endotoxin. J. Exp. Med. 185, 579–582 (1997). An early study showing that IL-1β is released from microglia by activation of purinergic, P2X7 receptors. Bacterial LPS is required for activation of microglial IL-1β expression, whereas ATP induced cleavage and release.
Ohtsuki, T., Ruetzler, C. A., Tasaki, K. & Hallenbeck, J. M. Interleukin-1 mediates induction of tolerance to global ischemia in gerbil hippocampal CA1 neurons. J. Cereb. Blood Flow Metab. 16, 1137–1142 (1996). The first demonstration that endogenous IL-1 can mediate ischaemic tolerance. Pre-treatment of gerbils three days before global ischaemia reduced brain injury. IL-1 was induced by a brief period of ‘preconditionary’ ischaemia.
Carrié, A. et al. A new member of the IL-1 receptor family highly expressed in hippocampus and involved in X-linked mental retardation. Nature Genet. 23, 25–31 (1999). A direct link between one of the recently identified members of the IL-1/Toll receptor family in brain function. Cognitive function in patients with X-linked mental retardation is strongly associated with a nonsense mutation in a gene identified as IL-1-receptor-like protein (IL-1R AcPL).
Venters, H. D. et al. A new mechanism of neurodegeneration: a proinflammatory cytokine inhibits receptor signaling by a survival peptide. Proc. Natl Acad. Sci. USA 96, 9879–9884 (1999). This study provided a potential explanation for indirect effects of the proinflammatory cytokine TNFα on neuronal survival through modification of the signalling pathway of a protective growth factor, IGF. This mechanism might apply to other neurotoxic cytokines.
Loddick, S. A., MacKenzie, A. & Rothwell, N. J. An ICE inhibitor, z-VAD-DCB attenuates ischaemic brain damage in the rat. Neuroreport 7, 1465–1468 (1996). The first study reporting that inhibition of caspase activity protects against neuronal death (ischaemic brain damage) in vivo
Legos, J. J. et al. SB 239063, a novel p38 inhibitor, attenuates early neuronal injury following ischemia. Brain Res. 892, 70–77 (2001). The first study to show that selective inhibition of p38 MAPK, which is involved in IL-1 and TNFα signalling,
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The nervous system does not function normally without Vitamin D. It is involved in the synthesis of neurotransmitters such as dopamine, serotonin, and acetylcholine. Vitamin D protects against inflammation in the brain, particularly in the hippocampus, which is important in memory.
Vitamin D injections lessen age-related inflammation and also improve age-related memory impairments. In particular, it augments the removal of beta-amyloid plaques found in Alzheimer’s disease.
There is a strong association between vitamin D level and the risk of Alzheimer’s disease. In particular, people deficient in Vitamin D (levels less than 20ng/ml) have a 53% increase risk of becoming demented, and a 69% increase risk of getting Alzheimer’s disease. In severe Vitamin D deficiency (levels less than 10 ng/ml), the chance of Alzheimer’s is 122%!
Recommended intake of Vitamin D per the Institute of Medicine is 600 IU/day of Vitamin D for age under 70, and 800 IU/day for age over 70.
There is evidence that you can safely take up to 4000 IU/day of Vitamin D.
As of yet, no single therapeutic intervention has been found to impact Alzheimer’s disease. Whereas other diseases, such as cancer and HIV treatment have required a multi-modal intervention, why shouldn’t Alzheimer’s?
Alzheimer’s disease (AD) results, in part, from a failure of synapse formation (called neuronal plasticity), which allows brain cells to connect with each other to preserve memory and basic functions. Instead, in AD, there is an increase in breakdown products on the right side of the diagram above, that cause less neurons to connect.
The goal of therapy may be to increase the trophic, anti-AD processing, leading to more neurons connecting and thus preventing Alzheimer’s disease. This requires multiple medicines and processes to intervene. and succeed.
A study listed in the link below demonstrated that using these interventions resulted in a reversal of memory loss and even a return to a employment in 10 individuals who followed the regimen. This reversal started in 3-6 months after initiation and remained for the duration of the study over two years.
Enhance ketogenesis by fasting 12 hours at night including three hours prior to bedtime. This reduces insulin levels and A-beta.
Reduce stress through meditation or yoga, thereby reducing cortisol levels and stress,
Optimize sleep – obtain 8 hours a night, use melatonin 0.5 mg at night and Tryptophan 500 mg three times a week. Get checked and treated for sleep apnea.
Exercise 30-60 minutes a day for four-six days a week.
Keep you brain active mentally through reading or mental exercises.
Maintain your homocysteine levels to <7 – using methylcobalamin 1mg a day, methyltetrahydrofolate 0.8 mg a day, and pyridoxine-5-phosphate 50 mg a day. Consider taking trimethylglycine.
Maintain serum B-12 above 500 by taking oral B-12 as above
Keep the CRP<1 ( inflammation marker) using an anti-inflammatory diet that includes curcumin, DHA (docosahexanoic acid) 320 mg and EPA (eicosapentanoic acid) 180 mg a day
Optimize fasting insulin <7 and keep the hemoglobin A1c <5.5 by following your diabetic diet precisely.
Optimize your hormone balance, including your free T3 and T4, and estradiol, and testosterone levels. Be certain cortisol and progesterone/pregnenolone levels are in range through lab tests.
GI health maintenance through probiotics use.
Reduce A-beta through the use of cucumin and herbs such as Ashwagandha (500mg a day) and Bacopa Monniera (250 mg a day) and tumeric 400 mg a day.
Cognitive enhancement through the use of Bacopa monniera and magnesium threonate.
Vitamin D3 needs to be between 50-100 ng/ml by appropriate Vitamin D3 intake ( up to 2000 IU/day) and Vitamin K2.
Increase NGF through intake of H. ernaceus or acetyl-L-carnitine.
Provide synaptic structural components through citicoline 500 mg twice a day and DHA (docosohexanoic acid) 320 mg a day.
Optimize antioxidants by intake of mixed tocopherols and tocotrienols, with selenium blueberries, n- acetyl cysteine, ascorbate, and alpha-lipoic acid. For example, use of vitamin C at 1 gram a day, Vitamin E at 400 IU a day, and alpha-lipoic acid a 100 mg a day.
Optimize the zinc and copper ratio: if needed, , zinc picolinate at 50 mg a day may be needed, depending on the zinc levels.
Treat sleep apnes as needed to maximize nighttime oxygenation.
Optimize mitochondrial function through CoQ10 at 200 mg a day, alpha lipoic acid at 100 mg a day, polyquinoline quinone, N-acetyl cysteine, acetyl-L-carnitine, zinc, resverarol, thiamine and Vitamin C intake.
Increase focus through pantothenic acid.
Increase SirT1 function through Resveratrol intake.
Exclude heavy metal toxicity and evaluate fo mercury, lead, cadmium toxicity.
Reduce mMCT effects (medium chain triglycerides – a part of our diet) by taking coconut oil at a teaspoon three times a day or using Axona.
Obviously multiple lab test parameters are needed to determine needs and the interventions are quite rigorous, requiring a strict diet and lots of pills throughout the day, but this multi-modal intervention seems to work!
Lab tests that may be needed include: serum homocysteine, CRP, Vitamin D levels, Hemoglobin A1c, serum copper, serum zinc, ceruplasmin, pregnenolone, testosterone level, albumin:globulin ratio, cholesterol, morning cortisol, free T3 and T4 and TSH levels, DHEA levels, estradiol level, progesterone, insulin.
It is extensive but this seems to hold promise. More later!
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