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The Ultimate Guide to Cellular Longevity: NAD+, Methylation, and Senolytics   
Date:
September 10, 2026 10:57 AM
Introduction: Understanding Cellular Aging and Energy DeclineBiological aging represents a progressive decline in cellular maintenance, structural repair, and energy generation. Over decades, tissues experience an attrition of functional reserves, compromised stress resilience, and persistent low-grade systemic inflammation. At the cellular scale, biological degeneration is driven by a failure to generate bioenergetic fuel, repair genetic code, and clear metabolic waste.Cellular aging is characterized by interconnected biological disruptions known as the hallmarks of aging. These encompass genomic instability, epigenetic alterations, mitochondrial decay, loss of proteostasis, and cellular senescence. Rather than operating as isolated occurrences, these phenomena establish a self-reinforcing degenerative cycle: declining cellular power generation impairs enzymatic genetic repair, promoting the accumulation of damaged cells that enter irreversible growth arrest and poison surrounding healthy tissues. Mitigating cellular aging requires examining how microscopic bioenergetic pathways deteriorate and evaluating how targeted nutritional and biochemical interventions can restore cellular homeostasis. The Role of Mitochondria and ATP ProductionEvery biological function - from muscular contraction to continuous DNA replication - depends on adenosine triphosphate (ATP), the primary biochemical energy currency of living systems. Cells produce the vast majority of this energy within mitochondria through oxidative phosphorylation. Within these specialized organelles, metabolic intermediates derived from dietary carbohydrates and lipids donate high-energy electrons to the electron transport chain. The flow of these electrons across protein complexes establishes an electrochemical proton gradient across the inner mitochondrial membrane, driving ATP synthase to manufacture ATP.A youthful cell functions like an efficient municipal power grid, dynamically matching energetic demands with immediate ATP output. However, as biological aging progresses, mitochondrial efficiency declines. The electron transport chain becomes structurally leaky, inadvertently shedding electrons that react with ambient molecular oxygen to produce reactive oxygen species (ROS). While regulated levels of ROS participate in vital intracellular signaling, chronic excess induces widespread oxidative stress. Mitochondria are exceptionally vulnerable to this oxidative burden because they carry their own circular genetic material, known as mitochondrial DNA (mtDNA). Unlike nuclear DNA, mtDNA lacks the protective shielding of histone proteins and possesses rudimentary repair systems. As a result, mtDNA sustains cumulative oxidative damage, encoding increasingly defective electron transport chain proteins. This dynamic generates a bioenergetic deficit: degraded mitochondria synthesize progressively less ATP while emitting greater volumes of damaging free radicals. Deprived of optimal ATP reserves, cells lack the energy necessary to drive vital enzymatic repair cascades, accelerating structural degeneration and functional exhaustion. How Cellular Senescence Accelerates the Aging ProcessWhen healthy cells confront critical physiological damage - such as severe telomere attrition, persistent DNA double-strand breaks, or oxidative stress - they activate protective cell cycle arrest pathways governed primarily by the p53/p21^CIP1 and p16^INK4a/Rb molecular checkpoints. This defensive shutdown, termed cellular senescence, permanently prevents the replication of potentially premalignant or mutated cells.Senescent cells, colloquially known as "zombie cells," enter a state of permanent growth arrest while actively resisting programmed cell death (apoptosis). Over time, these cells accumulate within adipose depots, skeletal muscle, the vascular endothelium, and major organs, largely because immune surveillance and clearance pathways simultaneously lose functional efficiency. The systemic danger of senescent cells stems from their secretome. Rather than remaining biologically inert, senescent cells develop a hyperactive secretory state termed the Senescence-Associated Secretory Phenotype (SASP). The SASP is a destructive mixture of pro-inflammatory cytokines, chemokines, extracellular matrix-degrading matrix metalloproteinases (MMPs), and reactive oxygen species. Through this toxic secretome, even a small burden of senescent cells can impair whole-tissue architecture. SASP factors degrade surrounding structural proteins, induce insulin resistance in neighboring metabolic cells, and biochemically force adjacent healthy cells into secondary senescence. This persistent paracrine signaling fuels chronic, sterile, low-grade systemic inflammation, termed "inflammaging," which accelerates systemic tissue degeneration and elevates susceptibility to degenerative age-related pathologies. Nicotinamide Riboside (NR) and the NAD+ Salvage PathwayThe Biochemistry of NAD+ Depletion Over TimeNicotinamide adenine dinucleotide (NAD+) is an indispensable coenzyme present in every living cell. NAD+ fulfills a dual biological mandate: it serves as a central redox cofactor that shuttles electrons between cellular metabolic reactions, and it functions as an obligatory consumable substrate for regulatory enzymes that preserve cellular viability. In its redox capacity, NAD+ accepts electrons to form NADH during glycolysis, the tricarboxylic acid (TCA) cycle, and fatty acid beta-oxidation, subsequently donating those electrons to Complex I of the respiratory chain to power ATP synthesis.
The primary enzymatic driver of age-related NAD+ destruction is CD38, a membrane-bound glycohydrolase expressed on immune cells that is upregulated in response to chronic SASP exposure. Concurrently, lifelong genotoxic damage causes persistent activation of Poly(ADP-ribose) polymerase 1 (PARP-1), an enzyme that cleaves the glycosidic bonds of NAD+ to assemble branched poly(ADP-ribose) chains at DNA lesion sites. Because PARP-1 consumes NAD+ without directly recycling the molecule, chronic DNA damage depletes intracellular NAD+ pools, impairing bioenergetics and limiting sirtuin activity. How NR Efficiently Boosts Cellular NAD+ LevelsThe mammalian body maintains its NAD+ supply through three distinct biosynthetic routes: the de novo pathway from dietary L-tryptophan, the Preiss-Handler pathway from nicotinic acid (niacin), and the NAD+ Salvage Pathway. The de novo pathway requires substantial energy expenditure, consuming roughly sixty milligrams of dietary tryptophan to yield a single milligram of NAD+. The Preiss-Handler pathway, while effective, can induce cutaneous prostaglandin-mediated flushing at therapeutic intakes. Consequently, the salvage pathway serves as the primary mechanism for maintaining intracellular NAD+ pools.The salvage pathway recycles the breakdown product nicotinamide (NAM), which is released whenever NAD+-consuming enzymes execute their functions. Under normal conditions, cells convert free nicotinamide into nicotinamide mononucleotide (NMN) via the rate-limiting enzyme nicotinamide phosphoribosyltransferase (NAMPT), after which NMN adenylyltransferases (NMNAT1–3) complete the conversion into NAD+. However, NAMPT expression declines with advancing age, chronic inflammation, and metabolic stress, limiting the recycling capacity of the cell. Nicotinamide Riboside (NR) is a naturally occurring pyridine nucleoside that bypasses this enzymatic bottleneck. Upon cellular entry via equilibrative nucleoside transporters, NR is directly phosphorylated into NMN by nicotinamide riboside kinases (NRK1 and NRK2) using a single molecule of ATP. Because the NRK pathway remains intact and robust across the lifespan, NR provides an efficient alternative entry point into the NAD+ salvage cascade. Clinical evaluations in humans confirm the safety, bioavailability, and pharmacokinetics of oral NR supplementation. Randomized, double-blind, placebo-controlled trials reveal that oral NR chloride produces dose-dependent increases in steady-state whole blood NAD+ concentrations. Dosing regimens of 100 mg, 300 mg, and 1,000 mg daily elevate blood NAD+ levels by approximately 22%, 51%, and up to 142%, respectively, within two weeks of administration, maintaining these elevations throughout continuous use. High-resolution metabolomic analyses also demonstrate parallel elevations in nicotinic acid adenine dinucleotide (NAAD), establishing it as a reliable biomarker of active intracellular NAD+ synthesis without hepatic or systemic toxicity. Sirtuin Activation and DNA Repair MechanismsReplenishing intracellular NAD+ supports functions beyond mitochondrial ATP generation. NAD+ functions as an obligatory cofactor for sirtuins (SIRT1 through SIRT7), a family of class III histone and non-histone protein deacetylases that regulate stress resilience, metabolic homeostasis, and cell survival. Sirtuins couple the removal of acetyl groups from target lysine residues to the stoichiometric cleavage of NAD+, producing nicotinamide and O-acetyl-ADP-ribose. In states of NAD+ deficiency, sirtuin enzymes remain inactive regardless of cellular demand.In the nucleus, SIRT1 coordinates defense against cellular decline. When activated by restored NAD+ levels, SIRT1 deacetylates peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1a), the master transcriptional coactivator of mitochondrial biogenesis. This deacetylation stimulates mitochondrial replication and assembly, expanding functional respiratory capacity. Concurrently, SIRT1 deacetylates the p65 subunit of nuclear factor-kappa B (NF-kB), suppressing the transcription of pro-inflammatory cytokines. In the mitochondria, SIRT3 utilizes NAD+ to deacetylate metabolic enzymes and superoxide dismutase 2 (SOD2), enhancing the organelle's capacity to neutralize reactive oxygen species. At the same time, cellular NAD+ levels directly regulate genomic integrity through PARP-1. When genotoxic stress or oxidative damage induces single- or double-strand DNA breaks, PARP-1 binds to the damaged termini using its zinc-finger domains. Bound PARP-1 hydrolyzes NAD+ to synthesize extensive, negatively charged poly(ADP-ribose) polymers on itself and adjacent histones. This modification relaxes chromatin architecture and establishes an electrostatic scaffold that recruits base excision repair and homologous recombination complexes. Recent discoveries demonstrate close crosstalk between sirtuins and PARP-1 during DNA repair. PARP-1 recruits SIRT1 to double-strand breaks, where SIRT1 deacetylates the chromatin-remodeling ATPase BRG1 to displace nucleosomes and facilitate homologous recombination. However, because PARP-1 and SIRT1 draw from the same intracellular NAD+ pool, severe NAD+ depletion forces a biological compromise: PARP-1 consumes the scarce remaining cofactor to address DNA damage, leaving sirtuins deactivated. Restoring NAD+ via NR prevents this deficit, enabling concurrent genomic repair and sirtuin-mediated metabolic defense. Quercetin: A Powerful Senolytic and mTOR RegulatorClearing Senescent "Zombie" Cells from TissuesThe accumulation of senescent cells has driven interest in senolytics: molecules that selectively eliminate senescent cells while sparing healthy, non-senescent populations. Senolytic agents exploit a specific vulnerability in senescent cells. Because senescent cells produce cytotoxic, pro-inflammatory SASP factors that would normally induce their own death, they become dependent on upregulated Senescent Cell Anti-Apoptotic Pathways (SCAPs) to survive. The SCAP network involves anti-apoptotic proteins (such as BCL-2 and BCL-xL), the PI3K/Akt kinase cascade, and cyclin-dependent kinase inhibitors.Quercetin is a polyphenolic flavonoid found in capers, red onions, apples, and the flower buds of Sophora japonica. Beyond its classical antioxidant properties, quercetin functions as a senolytic compound that exerts multi-target inhibitory effects across the SCAP network. By inhibiting the upstream PI3K/Akt survival axis and downregulating anti-apoptotic defenses, quercetin disrupts the signaling that protects senescent cells from intrinsic apoptosis. Deprived of these survival signals, senescent cells undergo programmed cell death. Preclinical studies demonstrate that senolytic protocols utilizing quercetin - often combined with the tyrosine kinase inhibitor dasatinib - reduce senescent cell burden across multiple tissues. This targeted clearance lowers circulating SASP factors, attenuates tissue fibrosis, restores endothelial reactivity, and improves functional health span. By removing senescent cells, quercetin mitigates the primary driver of chronic, low-grade inflammaging. Modulating the mTOR Pathway for Optimal AutophagyThe mechanistic Target of Rapamycin (mTOR) is an evolutionarily conserved serine/threonine protein kinase that coordinates cellular metabolism by balancing anabolic growth with catabolic recycling. Operating within two multiprotein complexes - mTORC1 and mTORC2 - the mTOR pathway integrates signals from amino acids, growth factors, and intracellular energy levels. In nutrient-rich environments, mTORC1 promotes protein synthesis, lipogenesis, and cellular growth, while suppressing catabolic breakdown. Conversely, nutrient scarcity downregulates mTORC1, activating autophagy.Autophagy is an intracellular degradation system that packages damaged organelles, misfolded protein aggregates, and biological debris into double-membraned autophagosomes for lysosomal degradation and recycling. A specialized branch of this pathway, mitophagy, selectively targets and clears damaged mitochondria. In modern metabolic conditions characterized by continuous caloric intake, mTORC1 can remain persistently active. This persistent signaling suppresses autophagy, causing damaged organelles and toxic aggregates to accumulate within tissues. Quercetin functions as a natural modulator of mTOR signaling. By inhibiting upstream PI3K/Akt signaling and activating intracellular energy sensors, quercetin attenuates overactive mTORC1, mimicking the metabolic effects of caloric restriction. This down-regulation relieves inhibition on the ULK1 autophagy initiation complex, stimulating both general autophagy and mitophagy. As autophagy proceeds, cells clear protein aggregates and eliminate damaged mitochondria, supporting cellular longevity and proteostasis. Enhancing Absorption: Phytosomes and Dietary FatsDespite the biological activities of quercetin identified in experimental models, its clinical translation has historically been limited by poor oral bioavailability. Raw quercetin aglycone is a crystalline, hydrophobic polyphenol with poor solubility in water and gastrointestinal fluids. When ingested in unformulated powder forms, quercetin molecules aggregate in the gut lumen, resisting dissolution and passive absorption. Consequently, the vast majority of an unformulated dose passes into the colon unabsorbed, where it undergoes microbial degradation without reaching meaningful systemic concentrations.To address these pharmacokinetic limitations, advanced delivery systems such as phytosomes were engineered. A phytosome is a 100% food-grade molecular complex where individual polyphenolic molecules are bound to dietary phospholipids, typically sunflower-derived phosphatidylcholine. Unlike a classical liposome - which encapsulates water-soluble compounds inside an aqueous core enclosed by a lipid bilayer - a phytosome forms an amphiphilic complex at the molecular level. The polar head of the phosphatidylcholine molecule forms hydrogen bonds with the hydroxyl groups of the quercetin molecule, while its lipophilic fatty acid tails extend outward. This structural arrangement shields the polar regions of the flavonoid, creating a lipid-compatible complex that integrates smoothly into the intestinal mucosa.
The Importance of Methylation in Healthy AgingVitamin B-Complex and Choline as Essential Methyl DonorsMethylation is an essential biochemical process occurring billions of times each second across all human tissues. It involves the transfer of a single-carbon unit - a methyl group consisting of one carbon atom bound to three hydrogen atoms - (CH3) - from a donor molecule to diverse recipients, including DNA, RNA, structural proteins, neurotransmitters, and membrane phospholipids. This transfer of one-carbon units is coordinated by the methionine-homocysteine cycle, which sustains genetic stability, detoxification pathways, and cellular repair.At the center of this pathway sits S-adenosylmethionine (SAM), the universal methyl donor in human biology. When a methyltransferase enzyme transfers a methyl group from SAM to an acceptor molecule, SAM is converted into S-adenosylhomocysteine (SAH). SAH functions as a potent competitive inhibitor of intracellular methyltransferases. To maintain functional methylation, SAH is rapidly hydrolyzed into homocysteine, a sulfur-containing amino acid that must be remethylated or cleared through transsulfuration. Homocysteine clearance proceeds through two distinct remethylation pathways. The primary route operates across most tissues via the enzyme methionine synthase, which requires vitamin B12 in its active methylcobalamin form. Methionine synthase transfers a methyl group from 5-methyltetrahydrofolate (5-MTHF, the active form of folate) to homocysteine, regenerating methionine. The ongoing production of 5-MTHF depends on the enzyme methylenetetrahydrofolate reductase (MTHFR), which utilizes riboflavin (vitamin B2) as a cofactor. Alternatively, excess homocysteine can be routed into the transsulfuration pathway by vitamin B6 (as pyridoxal-5'-phosphate) to synthesize cystathionine, cysteine, and ultimately the antioxidant glutathione. A secondary remethylation pathway, active predominantly in hepatic and renal tissues, bypasses folate entirely. In this route, dietary choline is oxidized to betaine (trimethylglycine or TMG). The enzyme betaine-homocysteine S-methyltransferase (BHMT) then transfers a methyl group from betaine directly to homocysteine, yielding methionine and dimethylglycine. When dietary intake of active B-vitamins or choline is insufficient, or when genetic variations like MTHFR polymorphisms reduce pathway flux, the methylation cycle slows. Homocysteine accumulates in circulation, promoting vascular and neurological inflammation, while SAM reserves decline, restricting cellular methylation capacity. Understanding DNA Methylation and Epigenetic HealthEvery somatic cell in an organism carries an identical genetic code. Cellular differentiation and tissue-specific functions are governed by the epigenome: a regulatory layer of chemical modifications that dictates gene expression without altering underlying DNA sequences. DNA methylation represents the primary and most stable epigenetic modification. In this process, DNA methyltransferase (DNMT) enzymes utilize methyl groups donated by SAM to add a methyl tag to cytosine bases adjacent to guanine residues, forming 5-methylcytosine within CpG dinucleotide sites.Under physiological conditions, DNA methylation maintains genomic stability and coordinates transcription. Methylation of promoter regions condenses chromatin, repressing transposable elements and silencing genes inappropriate for a given cell type. Conversely, hypomethylated promoters maintain an open chromatin state, allowing transcription factors to bind and initiate gene expression. During biological aging, this epigenetic landscape undergoes progressive dysregulation, a phenomenon termed "epigenetic drift". Aging cells experience global hypomethylation alongside focal hypermethylation of specific gene promoters. Global loss of methyl tags destabilizes the genome, activating retrotransposons and pro-inflammatory pathways. Simultaneously, hypermethylation at targeted promoter sites silences critical tumor suppressor genes and DNA repair complexes. This systematic change in DNA methylation patterns is consistent across populations, allowing researchers to develop molecular "epigenetic clocks". Algorithms such as the Horvath clock, PhenoAge, and GrimAge quantify biological age by profiling the methylation status of specific CpG sites across the genome. These clocks assess whether individuals are aging faster or slower than their chronological years. Ensuring a steady supply of methyl donors and preventing unnecessary SAM depletion supports DNMT activity, maintaining epigenetic patterns and genomic stability. How the Methylation Cycle Impacts Energy and Cognitive FocusBeyond long-term epigenetic regulation, the methylation cycle directly modulates immediate biochemical processes that govern daily energy, neurotransmission, and cognitive focus. Compromised methylation capacity frequently manifests as cognitive slowing, executive fatigue, and reduced physical stamina.A major consumer of methyl reserves is the endogenous synthesis of creatine. Approximately 40% of all SAM-derived methyl groups in the human body are utilized by guanidinoacetate N-methyltransferase (GAMT) in the liver to synthesize creatine. Creatine then translocates to the brain and skeletal muscle, where it is phosphorylated into phosphocreatine. Phosphocreatine functions as a rapid energy buffer, donating a high-energy phosphate group to regenerate ADP into ATP in milliseconds during demanding physical or cognitive tasks. When methyl donor availability falls, endogenous creatine synthesis drops, depleting phosphocreatine reserves and increasing susceptibility to neuromuscular and cognitive fatigue. Methylation is equally central to central nervous system architecture. SAM provides methyl groups to convert phosphatidylethanolamine into phosphatidylcholine, the predominant phospholipid comprising neuronal cell membranes and the myelin sheaths that insulate axons. Intact myelin preserves rapid action potential conduction throughout the nervous system. Furthermore, free choline derived from this pathway is the direct precursor to acetylcholine, the neurotransmitter required for attention, working memory, and learning. The methylation cycle also governs monoamine neurotransmitter metabolism. SAM is required for the synthesis of adrenaline (epinephrine) from noradrenaline, while catechol-O-methyltransferase (COMT) relies on SAM to degrade dopamine and norepinephrine within the prefrontal cortex. Sluggish methylation disrupts this balance, contributing to cognitive fatigue, mood variability, and impaired mental performance. Building a Comprehensive Longevity ProtocolSynergizing NR, Quercetin, and Methylated B-VitaminsLongevity supplementation often falters when single molecules are administered in isolation, ignoring interconnected metabolic pathways. Designing an effective cellular longevity protocol requires combining complementary mechanisms that reinforce one another while preventing secondary metabolic deficits. The combination of Nicotinamide Riboside, Quercetin Phytosome, and Methylated B-Vitamins illustrates this multi-target synergy.This synergy is grounded in the direct biochemical intersection between the NAD+ salvage pathway and the methylation cycle. When high-dose NR is supplemented to boost systemic NAD+, sirtuins and PARP enzymes consume the newly synthesized cofactor, generating substantial quantities of free nicotinamide (NAM). This intracellular nicotinamide faces two primary metabolic fates: it can be recycled back into NAD+ through the NAMPT-dependent salvage loop, or it can be cleared via methylation. When the influx of nicotinamide exceeds salvage recycling capacity, the excess is cleared to avoid feedback inhibition of sirtuin enzymes. To accomplish this, the enzyme nicotinamide N-methyltransferase (NNMT) transfers a methyl group from SAM directly onto nicotinamide, forming 1-methylnicotinamide (1-MNA/MNAM), which is subsequently excreted in urine. Prolonged, high-dose precursor administration without nutritional methyl support can elevate NNMT flux, depleting intracellular SAM reserves. As methyl groups are consumed clearing nicotinamide, the cellular SAM-to-SAH ratio falls, which can elevate circulating homocysteine and reduce methyl availability for DNA methylation and neurotransmitter synthesis. Co-administering a fully methylated B-complex alongside choline or betaine addresses this potential bottleneck. Providing active methyl donors (such as 5-MTHF, methylcobalamin, and betaine) maintains the one-carbon donor pool. Even during increased NNMT activity, SAM pools remain stable, protecting DNA methylation fidelity and maintaining homocysteine within safe parameters. Quercetin reinforces this protocol through complementary mechanisms. By clearing senescent cells and reducing SASP-mediated inflammation, quercetin downregulates CD38, the primary enzyme responsible for age-related NAD+ degradation. Suppressing CD38 prevents unnecessary breakdown of newly synthesized NAD+, enhancing the efficiency of NR supplementation. Furthermore, while NR provides the NAD+ necessary to activate SIRT1-driven mitochondrial biogenesis, quercetin concurrently modulates mTORC1 to stimulate autophagy. This coordinated action ensures that newly generated mitochondria operate in an environment cleared of proteotoxic cellular debris. The Crucial Role of Magnesium Glycinate and Zinc in Cellular FunctionLongevity protocols require essential mineral cofactors to function efficiently. Without adequate divalent minerals acting as enzymatic cofactors and structural stabilizers, metabolic longevity pathways cannot operate at full capacity. Among these, magnesium and zinc are required for cellular repair, genomic stability, and energy production.Magnesium serves as an obligatory cofactor in over 300 enzymatic reactions, primarily through its interaction with ATP. In biological systems, ATP exists predominantly as a chelate with a divalent magnesium ion, forming biologically active Mg2+ -ATP. Every enzymatic reaction that synthesizes, transfers, or consumes cellular energy - including the enzymes of the NAD+ salvage pathway (NRK and NMNAT) and DNA polymerases - strictly requires Mg2+ -ATP as its substrate. Magnesium deficiency impairs these phosphorylation reactions, reducing the cellular utilization of NAD+ precursors. Additionally, magnesium is an essential cofactor for the enzymes that activate dietary B-vitamins into their active forms. Supplying magnesium as magnesium glycinate provides high gastrointestinal bioavailability, minimal laxative effect, and yields glycine to support inhibitory neurotransmission and restful sleep. Zinc serves as a vital structural component for more than 3,000 human transcription factors and enzymatic proteins. Its most prominent structural role in longevity occurs within zinc-finger motifs. These are specialized protein conformations stabilized by a zinc ion coordinated to cysteine and histidine residues. The DNA damage sensor PARP-1 utilizes three zinc-finger domains to identify, track, and physically bind to single- and double-strand DNA breaks. Without adequate intracellular zinc, PARP-1 cannot properly assemble or dock onto damaged chromosomes, impairing DNA repair and increasing genomic instability. Zinc is also an obligatory structural component of copper/zinc superoxide dismutase (Cu/Zn-SOD or SOD1), the primary cytosolic antioxidant enzyme that dismutates superoxide radicals into hydrogen peroxide, protecting mitochondrial membranes and nuclear DNA from premature senescence. Integrating Prebiotics (like Acacia and Inulin) for Gut-Derived Longevity MarkersA comprehensive cellular longevity framework must extend beyond somatic tissues to encompass the gut microbiome. The intestinal microbiome functions as a central regulator of systemic inflammatory tone, immune development, and metabolic signaling. Age-associated dysbiosis - characterized by the loss of beneficial commensals and an overgrowth of pathobionts - frequently leads to breakdown of the intestinal barrier.The gut epithelium consists of a single-cell monolayer sealed by tight junction proteins, including zonula occludens-1 (ZO-1), occludin, and claudins. When this physical barrier is disrupted by poor dietary fiber intake or dysbiosis, gut permeability increases. This allows lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria, to enter the portal and systemic circulation. The resulting "metabolic endotoxemia" activates Toll-like receptor 4 (TLR4) on immune cells, inducing NF-kB and systemic pro-inflammatory cytokine production. This persistent gut-derived inflammation exacerbates the SASP, accelerates tissue senescence, upregulates CD38, and drains systemic NAD+ reserves.
These short-chain fatty acids, particularly butyrate, exert direct protective effects on systemic longevity. Butyrate provides the primary metabolic fuel for colonic epithelial cells, supplying more than 70% of their baseline energy needs and supporting mitochondrial function within colonocytes. Furthermore, SCFAs upregulate the expression of epithelial tight junction proteins (ZO-1, occludin, and claudin-1), restoring intestinal barrier integrity and preventing the translocation of inflammatory LPS into systemic circulation. Systemically absorbed butyrate also functions as an endogenous histone deacetylase (HDAC) inhibitor, suppressing pro-inflammatory gene expression and supporting regulatory T cell (T_reg) development. Reducing metabolic endotoxemia dampens systemic inflammation, protecting vascular function and preventing premature NAD+ depletion. Conclusion: The Integrated Cellular Longevity MatrixCellular longevity is achieved not by addressing isolated biomarkers in isolation, but by systematically supporting interconnected biological pathways. As bioenergetic capacity declines, cellular senescence accelerates, epigenetic patterns degrade, and gut barrier integrity weakens. A comprehensive approach addresses these biological vulnerabilities simultaneously.
Quercetin Phytosome clears senescent cells and modulates mTORC1, stimulating autophagy while dampening the inflammatory SASP cascade that accelerates CD38-mediated NAD+ destruction. Methylated B-vitamins, active folate, and choline replenish SAM reserves, balancing the methyl requirements of NNMT-mediated nicotinamide clearance, preserving epigenetic DNA methylation, and maintaining neurotransmitter production. Magnesium glycinate and zinc provide the structural and catalytic foundation required for ATP utilization, B-vitamin activation, and PARP-1 zinc-finger DNA repair docking. Finally, prebiotic fibers generate short-chain fatty acids like butyrate, reinforcing the intestinal barrier and preventing metabolic endotoxemia from fueling systemic inflammation. By coordinating energy replenishment, cellular waste clearance, epigenetic maintenance, and the suppression of systemic inflammation, this unified approach directly addresses the underlying drivers of cellular aging to support long-term physiological vitality.
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(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6650) Boost Memory 
Date:
March 23, 2009 01:56 PM
Our memory is as natural to us as breathing. An ability we all have, but don’t often think of, it doesn’t seem to cross our mind until we perceive that we are losing the ability. Memory lapses are an annoyance in themselves, but the anxiety that often comes along with them seems to be even worse. We often wonder if our memory problems are a symptom of some other problem like Midlife depression, arteriosclerosis, or even Alzheimer’s disease. Although Alzheimer’s disease is a fairly common disorder among older people, one must realize that most memory lapses have nothing to do with Alzheimer’s disease. Generally, it is believed that increasing age brings about an increased likelihood of developing memory loss. The mildest form of this illness is called age-associated memory impairment. This is characterized by one’s perception of his or her own memory loss and it is estimated that it is experienced by 40 percent of Americans over the age of sixty-five. Not all memory loss is attributable to aging, as occasional memory lapses are a natural normal part of life at almost any age, and are not likely to precede serious memory loss. With a proper diet, nutrition, and memory use, the memory should remain sharp and active well into one’s nineties or beyond. One big reason why people suffer from memory loss is an insufficient supply of necessary nutrients to the brain. The life of the body is in the blood, as it literally feeds and nourishes every cell within our bodies. Only certain substances are allowed to pass from the bloodstream into the brain, thanks to the protective envelope that is known as the blood-brain barrier. If the blood is thick with cholesterol and triglycerides, the amount of nutrient-rich blood that can pass through the blood-brain barrier decreases. This can result in the brain becoming malnourished over time. The functioning of the brain also depends upon substances that are referred to as neurotransmitters, which are brain chemicals that act as electrical switches in the brain and are responsible for all the functions of the body. If the brain does not have an adequate supply of neurotransmitters, or the nutrients to make them, it starts to develop something similar to a power failure or a short circuit. If you are trying to recall as specific fact or piece of information and your mind goes blank, it is likely that the above “short circuit” has occurred. There are many other factors that are involved in the deterioration of the memory. One of the most important is exposure to free radicals, which can cause huge amounts of damage if the memory is unchecked. Alcoholics and drug addicts often suffer a great deal of memory loss, with alcoholics being notorious for huge memory gaps that occur even though they are conscious. Allergies, candidiasis, stress, thyroid disorders, and poor circulation to the brain can also contribute to memory loss, while hypoglycemia can play a role in memory loss as well, as the brain requires that the level of glucose in the blood fall within a specific narrow range. Wide swings in blood sugar levels affect brain function and memory. The following nutrients are beneficial in dealing with and preventing memory loss: acetylcholine, boron, DMAE, garlic, huperzine A, lecithin granules, manganese, multivitamin and mineral complex, omega-3 fatty acid complex, phosphatidyl choline, phosphatidyl serine, SOD, vitamin A, vitamin B complex, vitamin B3, vitamin C, vitamin E, zinc, acetyl-l-carnitine, l-glutamine, l-tyrosine, coenzyme Q10, DHEA, DMG, melatonin, NADH, pregnenolone, RNA and DNA, Brahmi, ginkgo biloba, anise, blue cohosh, ginseng, gotu kola, and rosemary. All of the above mentioned as well as formulas tailored to help improve memory can be found in capsule, table, or power forms. Remember, only look to name brands such as Solaray, Source Naturals and Natures Plus for quality products. Memory vitamins and herbs can be found at your local or internet health food store. *Statements contained herein have not been evaluated by the Food and Drug Administration. Vitamins and herbs are not intended to diagnose, treat and cure or prevent disease. Always consult with your professional health care provider before changing any medication or adding Vitamins to medications.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=1981) The Essential Woman - Beauty and Balance from Within
Date:
August 13, 2005 02:25 PM
The Essential Woman - Beauty and Balance from WithinOutward Beauty is a reflection of inner health. Radiant glowing skin, lustrous hair, and strong nails are signs of vibrant inner health. Feminizing hormones, delicately balanced, provide freedom from monthly or Midlife female discomforts and beauty in full bloom. The Essential Woman is derived from seeds of botanical flowers such as evening primrose and flax, as well as special plant phyto-nutrients, all recognized for their beautifying and balancing qualities. Hallmarks of The Essential Woman:
The Essential Woman is available in liquid and capsules, and can be found in finer health food stores nationwide.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=731) Moderating Male Midlife Moodiness - The lesser known guy version of menopause is now a ...
Date:
July 14, 2005 09:28 AM
Moderating Male Midlife MoodinessThe lesser known guy version of menopause is now a syndrome
Question: How can you tell if a man has irritable male syndrome? Irritable male syndrome (IMS) may sound like a joke, but it's really no laughing matter. Just as women experience anxiety, depression and irritability with hormonal changes, men too can suffer from cyclic and menopausal symptoms-they're just more likely to be chastised for it instead of being consoled with a pint of Ben & Jerry's ice cream. Since men's hormones actually fluctuate every hour rather than every 28 days, it should come as no surprise that male behavior should be affected. For some men over 40, however, the behavior swing can be quite dramatic, leaving a guy in a chronic bad mood. But try telling the grouch that he suffers from "male menopause" and he just might chuck the Ben & Jerry's at you. The term "irritable male syndrome" was coined by Gerald A. Lincoln, a researcher at the Medical Research Council's Human Reproductive Sciences Unit in Edinburgh, Scotland. Lincoln first observed IMS while studying Soay sheep, a large, curly-horned variety known for their boisterous rutting rituals that rival the masculine intensity of any Super Bowl party. After mating season, however, Lincoln noticed that as testosterone levels dropped off, the rams became agitated, fearful, withdrawn and likely to irrationally strike out at other males. The hypothesis behind this behavior is that the withdrawal of androgens affects melatonin and serotonin uptake and can make for one cranky ram. However, IMS in two-legged, human subjects can present itself with more complexity. Psychotherapist Jed Diamond, author of The Irritable Male Syndrome: Managing the Four Key Causes of Depression and Aggression (Rodale Books), defines IMS as "a state of hypersensitivity, anxiety, frustration and anger that occurs in males and is associated with biochemical changes, hormonal fluctuations, and loss of male identity" that can occur at any time during a man's life. A lot of IMS involves depression; normally thought of as a female problem, this emotional downer often comes out differently in men, more outwardly than inwardly directed. One point of similarity between the sexes is that IMS, like depression in women, is often linked to the multi-source stress that pervades modern living. The result? According to Diamon, "Up to 30% of men, especially those in adolescence and Midlife, exhibit symptoms of IMS. In its mildest forms, it can cause men to be moody and irritable. At its worst, it can lead to violence and even suicide." Is it a Bad Day or a Bad Decade? So how can you really tell if a man has irritable male syndrome? Since a guy isn't likely to say flat out that he's having trouble with relationships or is having hot flashes (you read that right), there are other, more telltale signs to look for. While we all may temporarily experience bad moods, if you or someone you know exhibits one or more of these feelings with frequency over a period of time, IMS may be the cause: anger, sarcasm, defensiveness, blaming, withdrawal, anxiety, defiance, being argumentative, feeling unappreciated, frustration. Physical IMS symptoms include fatigue, unexpected weight gain or loss, frequent urination, hair loss (besides the typical male pattern) and impotence. The thyroid gland, which serves as the body's master energy controller, is often out of whack on men suffering from IMS. If that sounds familiar, see your practitioner for a thyroid hormone check. Less Flabby Means Less Crabby Sometimes, IMS is not a matter of lowered testosterone levels but one of elevated estradoil, the usable form of the female hormone estrogen. This condition can develop with consumption of too many hormone-laced meats (eating organic meat is a good option). In addition, a diet high in high-glycemic carbs such as white breads and white pasta will undermine testosterone levels as well as pack on unwanted pounds. To help trim down and keep IMS symptoms at bay, Larrian Gillespie, MD, author of The Gladiator Diet: How to Preserve Peak Health, Sexual Energy, and A Strong Body at Any Age (Healthy Life Publications), recommends a diet that's 40% protein, 35% low-glycemic carbs (read: green veggies) and 25% fat, of which only 10% should be saturated fat. To help keep testosterone levels up, avoid apricots, carrots, white potatoes, white rice (whole wheat past and rise are okay) and-sorry guys-dark beer. Gillespie also recommends that men take a multivitamin daily along with calcium, magnesium and the herb saw palmetto to inhibit the breakdown of testosterone into dihydrotestosterone a precursor to prostate disease. Now that you know IMS is real, you can take the bull (or Soay ram) by the horns and do something about it. IMS can be treated through diet, natural hormone replacement therapy and counseling, if necessary.
Question: What do you call a man who is always tired, miserable and irritable? Wrong answer! That was the old guy. Mr. Nice is back. -Karyn Maier
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=614) Women and Depression!
Date:
June 13, 2005 07:48 PM
Women and Depression by Lisa James Energy Times, March 11, 2004 Just as fog veils a beautiful landscape, so depression veils life itself: rendering existence dark and dreary, narrowing the scope of one's dreams. And women are particularly prone to this lingering sadness. The good news: Depression doesn't have to linger forever. With proper nutrition, lifestyle changes and a revived outlook, you can break through that fog into a sunnier emotional clime. Women are more likely than men to fall prey to depression throughout their lifetimes, with women being twice as likely as men to experience major depression. While the greatest risk for both sexes falls at Midlife, the gender difference appears early; one in ten teenage girls was found to suffer from major depression in one study (International Journal of Behavioral Development 2004; 28:16-25). What's more, childhood depression leaves a person more susceptible to mood problems in adulthood. One reason for the gender difference in depression, according to researchers, is that women tend to dwell on depressed feelings to a greater degree than men. Some scientists believe a family history of depression carries greater weight for women. Others theorize that the inner fluctuations of a woman's monthly cycle can leave her susceptible to stresses emanating from the outer world. Studies indicate that almost three-quarters of all premenstrual women experience some level of mood difficulties (Summit on Women and Depression, APA, April 02), and a woman's hormonal ebb and flow may even make her more vulnerable to seasonal affective disorder (SAD), the kind of depression linked to a lack of natural light. Warning Signs Not surprisingly, many depressed folks feel sad and lethargic, down on themselves and the world. But in some people, depression is marked by agitation and concentration difficulties, or is accompanied by anxiety. Sleep disturbances-either insomnia or excessive sleepiness-often ensue, and activities that used to provide pleasure lose their appeal. Breaking depression's grip can do more than just lighten your mood-it may help safeguard your health. Studies suggest depression dampens the immune response and may increase the risks of coronary heart disease and diabetes (Archives of General Psychiatry 2003; 60:1009-14; Circulation 2000; 102:1773; Diabetes Care 2004; 27:129-33). Origins of Depression The reasons some people are pulled down by depression's undertow while others are able to stay afloat emotionally are complex, but researchers believe common factors link them all. One factor that can't be ignored is genetics. "If you are depressed, there is a 25% chance that a first-degree relative-a parent, child or sibling-is also depressed," says Hyla Cass, MD, author of St. John's Wort: Nature's Blues Buster (Avery). Other factors are physical problems and medication side effects. That's why your first step should be a consultation with your health care practitioner (if your moods are especially dark, seek professional assistance as soon as possible). Life's worries and cares also weigh more heavily on some people than on others. " [N]ot only will certain stressors [adverse events] cause depression as a direct response," notes Dr. Cass, "but they may predispose an individual to future episodes of depression." For example, the end of a relationship when you feel you've lost a lover and been humiliated (and been cheated on) raises your risk of depression (Archives of General Psychiatry 2003; 60:789-96). The Depressed Brain When depression hits, brain chemistry shifts. As a result, chemicals known as neurotransmitters, which relay messages between brain cells, go awry. For instance, a neurotransmitter called serotonin-critical to mood control-may decrease, leaving you feeling depressed, anxious, craving certain foods and unable to sleep. Conversely, "high levels of serotonin are associated with emotional and social stability," according to Dr. Cass. She adds that, in addition, sex hormones such as estrogen and testosterone "affect brain cells directly." Lifting the Fog Because the causes of depression are so complex, leaving the darkness behind generally requires opening up several pathways. Part of feeling better simply lies in believing that you can. Researchers have found that depressed people who feel they have a sense of control over their troubles, do, in fact, have a better chance of recovery (General Hospital Psychiatry 2000; 22(4):242-50). Finding a community of like-minded folks bolsters your capacity to deal with mood problems. In some cases, time spent with a therapist can be a valuable aid in figuring out what's bothering you. On the physical side, losing weight can lift your spirits. Among women with severe obesity-itself a depression risk factor-losing weight has led to depression relief (Archives of Internal Medicine 2003; 163:2058-65). Research also indicates that exercise helps brighten dark moods. Nutritional Uplift A change in diet, along with certain supplements, can also help dispel depression. The first step on the road to emotional recovery: eat a lot of fresh, organic fruits and vegetables, and stay away from overly refined foods with high levels of sugar. Omega-3 fatty acids, the kinds found in flax seed and fish, are essential to proper brain function. In several studies, people who took supplemental omega-3s found significant relief from depression. Key amino acids-the basic units of which proteins are built-serve as starting points for the production of mood-lifting neurotransmitters. In one trial, people who took an amino-acid mix that included tyrosine enjoyed better moods and were happier than people who took amino acids without it (Psychopharmacology (Berlin) Sept 4 2003). Along with amino acids, the body needs the right vitamins-especially members of the all-important B family-to create depression-fighting brain chemicals. In one study, people with depression who took vitamin B12 improved their chances of recovery (BMC Psychiatry 2003; 3:17). Another interesting observation: Vitamin B12 and its partners vitamin B6 and folate are essential to keep a protein called homocysteine (known primarily as a cardiovascular hazard) from reaching excessive levels, and people with high homocysteine are twice as likely to be depressed. This has led some researchers to speculate that folate may help keep depression under control (Archives of General Psychiatry 2003; 60:618-26). Herbs that may help beat back the blues include two that help the body deal with stress, eleuthero (Eleutherococcus senticosus) and schisandra (S. chinensis). A new diet, a new outlook: With the help of the right nutrients and the right support, you can break the bonds of depression.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=336) Celebrating Women: Age Is Just a Number
Date:
June 13, 2005 07:43 PM
Celebrating Women: Age Is Just a Number by Carl Lowe Energy Times, March 10, 2004 As women age, their physical needs shift. The health challenges that face a woman in her thirties do not match those of a woman in her fifties. At the same time, some basic health needs stay constant: At any age, every woman requires a wealth of vitamins, minerals and the other natural chemicals that fruits, vegetables and supplements supply. She also constantly needs families and friends to support her spiritual health. As the internal workings of your body alter, your lifestyle must stay abreast of those adjustments. Peak health demands a finely tuned health program designed with your individual needs-and your stage of life-in mind. Ages 30 to 45 When it comes to maintaining health, younger women might seem to have it easier than older women. If they exercise and stay in shape, they maintain more stamina than women 10 to 20 years their senior. Unfortunately, many women in this age group mistakenly think they don't have to be as careful about their lifestyle habits and their eating habits as they will in later decades. But even if your health doesn't seem to suffer from poor eating choices or a sedentary lifestyle right away, your foundation for health in later life suffers if you don't care for yourself now. By age 45 you should have established the good habits that will carry you successfully through the aging process. As an added bonus, good lifestyle habits pay immediate dividends. If you pay attention to your nutrients and get plenty of physical activity when younger, you'll feel more energetic and probably enjoy better emotional health. Set Health Goals According to Gayle Reichler, MS, RD, CDN, in her book Active Wellness (Avery/Penguin), good health at any age doesn't just come to you-you have to plan for it. In order to stick to good habits, she says, "living a healthy lifestyle needs to be satisfying." Reichler believes that you need to picture your health goals to achieve them: "Every successful endeavor first begins in the mind as an idea, a thought, a dream, a conviction." Good health at this age and in later years requires a concrete strategy and visualization of how your body can improve with a healthy lifestyle. Your long-term health goals at this age should include an exercise program that will allow you to reach a physically fit old age with a lowered risk of disability. In addition, your short-term plans should encompass losing weight, staying optimistic, living life with more vim and vigor, increasing your capacity for exercise and lowering your stress. As Reichler points out, "Your long-term goal and your ideal vision establish what you want to achieve....[You should do] something good...for yourself every day and every week that makes your life easier and more consistent with your goals." Develop an Eating Plan Today, the average American gains about two pounds annually. As a result, every year a greater portion of the US population is obese and overweight. By controlling your food intake earlier in life, you may be able to avoid this weight gain. In his book Prolonging Health (Hampton Roads), James Williams, OMD, recommends basic changes to your diet that can provide long-term support of your health: Get Supplemental Help If you're in your thirties or forties and you don't take at least a multivitamin, start taking one today! A large body of research shows that taking vitamin and mineral supplements over a long period of time significantly supports better health. Calcium and vitamin D are two of the most important supplemental nutrients, helping to build stronger bones now that can withstand the bone-loss effects of aging. Calcium can also help keep your weight down. One study of younger women found that for every extra 300 milligrams of calcium a day they consumed, they weighed about two pounds less (Experimental Biology 2003 meeting, San Diego). In the same way, taking vitamin D supplements not only helps strengthen your bones, it can also lower your risk of multiple sclerosis (Neurology 1/13/04). In this study, which looked at the health records of more than 180,000 women for up to 20 years, taking D supplements dropped the chances of multiple sclerosis (although eating vitamin D-rich foods did not have the same benefit). And if you're thinking about having children at this age, a multivitamin is crucial for lowering your baby's risk of birth defects and other health problems. A study at the University of North Carolina at Chapel Hill found that women who take multivitamins during pregnancy lower their children's risk of nervous system cancer by up to 40% (Epidemiology 9/02). " Our finding, combined with previous work on reducing several birth defects with vitamin supplementation and other childhood cancers, supports the recommendation that mothers' vitamin use before and during pregnancy may benefit their babies' health," says Andrew F. Olshan, MD, professor of epidemiology at the UNC School of Public Health. "We believe physicians and other health care providers should continue to educate women about these benefits and recommend appropriate dietary habits and daily dietary supplements." In particular, Dr. Olshan feels that folic acid (one of the B vitamins), and vitamins C and A, are particularly important for lowering the risk of childhood cancers and birth defects. Ages 45 to 55 When you reach this in-between age-the time when most women have moved past childbearing age but haven't usually fully moved into the post-menopausal stage-you enjoy a propitious opportunity to take stock of your health and plan for an even healthier future. One thing that may need adjustment is your sleep habits, as sleeplessness is a common problem for women in this age group. Even if you haven't been exercising or watching your diet until now, it's not too late to start. Making lifestyle changes at this age can still improve your chances for aging successfully. For instance, it is at these ages that women should have their heart health checked. Research published in the journal Stroke (5/01) shows that having your cholesterol and blood pressure checked at this time more accurately shows your future chances of heart disease than having it checked at a later date after menopause, in your late fifties. " The premenopausal risk factors may be a stronger predictor of carotid atherosclerosis [artery blockages] because they represent cumulative risk factor exposure during the premenopausal years, whereas the risk factors...during the early postmenopausal years have a shorter time for influence," says Karen A. Matthews, PhD, a professor at the University of Pittsburgh Medical Center. In other words, Dr. Matthews' research shows that if you have high blood pressure and high cholesterol before menopause, you are at serious risk for a stroke or heart attack soon after menopause: These are important reasons that you need to start improving your health habits immediately. Increase in Heart Disease Before menopause, a woman's hormones and other physiological characteristics usually hold down her chance of heart disease. After menopause, when hormones and other bodily changes occur, the risk of heart attacks and stroke in women rises significantly. (Heart disease is the leading killer of women.) At least part of this increased risk is linked to the postmenopausal decrease in estrogen production. Dr. Matthews studied about 370 women in their late forties, measuring their weight, their BMI (body mass index, an indication of body fat compared to height), blood pressure, cholesterol and blood sugar. Ten years later, after the women had entered menopause, she and her fellow scientists used ultrasound to measure blockages in these women's neck arteries (a sign of heart disease). The researchers found that indications of potential heart problems (such as high blood pressure, high cholesterol and being overweight) when women were in their forties did indeed forecast future difficulties. " Women who had elevated cholesterol, higher blood pressures and increased body weight before menopause had increased blood vessel thickening and atherosclerotic plaque formation in the neck arteries after menopause. Such changes in the carotid arteries are associated with an increased heart attack and stroke risk," says Dr. Matthews. Heart Health Factors The four main lifestyle factors you should adjust at this age to support better heart function are diet, stress, exercise and weight. According to Dr. James Williams, "[M]ore than any other cause, dietary factors are the most critical factor in cardiovascular disease." He recommends eliminating "dietary saturated fatty acids as found in flame-broiled and fried meats." He also urges women to eat more fish and poultry, consume organic fruits and vegetables and cut back on refined sugar. Stress becomes an ever more important heart disease factor at this age as estrogen begins to drop. " Our study [in the lab] indicates that stress affects estrogen levels and can lead to the development of heart disease-even before menopause," says Jay Kaplan, PhD, of the Wake Forest University Baptist Medical Center (The Green Journal 3/02). Dr. Kaplan's research shows that stress in women ages 45 to 55 may reduce estrogen earlier in life and make women more susceptible to the arterial blockages that lead to heart disease. "We know from [lab] studies that stress can lower estrogen levels to the point that health is affected," he says. Stress can also hurt bone health: In a study of 66 women with normal-length menstrual periods, estrogen levels were low enough in half of the women to cause bone loss, making the women susceptible to osteoporosis. Exercise and Weight Although exercise used to be considered to be mainly a young woman's activity, the thrust of recent research suggests that physical activity actually becomes more important to health as you get older. A 17-year study of about 10,000 Americans found that exercising and keeping your weight down is probably the most important thing you can do to lower your risk of heart disease as you enter your forties and fifties (Am J Prev Med 11/03). Of the people who took part in this study, more than 1,500 people died of heart disease. Those who performed the most exercise were thinner and had a 50% chance less of dying of heart disease than overweight nonexercisers. " The fact is that those who both exercised more and ate more nevertheless had low cardiovascular mortality," says Jing Fang, MD, a researcher at the Albert Einstein College of Medicine in the Bronx, New York. An added benefit of exercise: If you burn up calories exercising, you can eat more and not have to worry as much about being overweight. Supplements and Diet If you're a woman at Midlife, a multivitamin and mineral is still good nutritional insurance. Eating plenty of fruits and vegetables are also important for getting enough phytochemicals, the health substances in plants that convey a wealth of health benefits. As you enter this age group, your immune system gradually slows down. To help support immune function, eating produce rich in antioxidant nutrients, and supplementing with antioxidants like vitamins C and E as well as carotenoids, can be especially important. For example, a study of people with ulcers found that people with less vitamin C in their stomachs are more likely to be infected with Helicobacter pylori, the bacteria that can cause peptic ulcers and is linked to stomach cancer (J Amer Coll Nutr 8/1/03). This research, which looked at the health of about 7,000 people, found that vitamin C probably helps the immune system fend off this bacterial infection. " Current public health recommendations for Americans are to eat five or more servings of fresh fruits and vegetables a day to help prevent heart disease, cancer and other chronic diseases," says Joel A. Simon, MD, MPH, professor of medicine at the University of California at San Francisco. Calcium and Bones At Midlife, calcium continues to be a vital mineral for supporting bone health. According to Gameil T. Fouad, PhD, "It has been routinely shown that a woman's calcium status and level of physical activity (specifically, the degree to which she participates in weight-bearing exercise) are positively associated with bone mineral density. It is less well appreciated that this is a process which takes place over the course of a lifetime." Dr. Fouad adds that calcium works in concert with other vitamins and minerals to keep bones healthy: "Research in the United Kingdom involving nearly 1,000 premenopausal women over age 40 illustrates those women with the highest bone density tended to have the highest intake of calcium. Surprisingly, this study also demonstrated that calcium does not act alone: those women with the best bone health also had the highest intakes of zinc, magnesium and potassium." Dr. Fouad stresses that supplements should go together with a lifestyle that includes enough sleep and exercise to help the body stay in top shape. " As a general guideline," he says, "a woman concerned with her mineral intake should take concrete steps to make sure she is getting adequate rest, is eating a well-balanced diet focused on fresh fruits, vegetables and lean protein as well as getting adequate exercise....A multi-mineral containing bio-available forms of zinc, magnesium, copper and selenium is probably a safe addition to anyone's routine. Taking these proactive steps dramatically reduces the chances that deficiencies will arise." Ages 55 and Beyond Entering the post-menopausal phase of life can present challenging opportunities for a new perspective on life and health. While some signs of aging are inevitable, experts who have looked at how the human body changes with age are now convinced that healthy lifestyle habits can improve how well you can think, move and enjoy life well past age 55. As Dr. Williams notes, "In your fifties, the force of aging is undeniably present: Your body shape changes and organ function declines, both men and women have a tendency to gain weight....Heart disease becomes more common, energy and endurance are considerably reduced and your memory begins to slip." But Dr. Williams also points out that you don't have to age as rapidly as other people do. He believes you should employ a "natural longevity program...[that starts] to reverse the course of aging as early as possible." One key to staying vital as you age is your outlook on life, an aspect of life that's greatly enhanced by strong social ties. Avoiding the Aging Slowdown The latest research shows that one of the most crucial ways to slow the effects of aging is to exercise and keep your weight down. It won't necessarily be easy, though. The change in hormonal balance at this age makes the body more prone to extra pounds (Society for Neuroscience Meeting, 11/12/03). " In women, it has been demonstrated that major weight increases often occur during menopause, the time in a woman's life in which cyclic ovarian function ends and the ovarian hormones estrogen and progesterone decline," says Judy Cameron, PhD, a scientist in the divisions of reproductive sciences and neuroscience at the Oregon Health & Science University. In Dr. Cameron's lab trials, she has found that the decrease in estrogen after menopause "resulted in a 67% jump in food intake and a 5% jump in weight in a matter of weeks." In other words, the hormonal changes you undergo as enter your late fifties causes your appetite to grow as well as your waistline: Developments that increase your chances of heart disease, cancer, diabetes, stroke and joint problems. Vigilance against this weight gain is necessary to save your health: Start walking and exercising. Research on exercise in people aged 58 to 78 found that getting off the couch for a walk or other physical activity not only helps control weight but also helps sharpen your thinking and helps you become more decisive (Proceedings of the National Academy of Sciences, 2/16-20/04, online edition). This recent study, done at the University of Illinois at Urbana-Champaign, found that performing aerobic exercise improved mental functioning by 11% (on a computer test). " We continue to find a number of cognitive benefits in the aerobic group," says Arthur F. Kramer, PhD, a professor of psychology at the Beckman Institute for Advanced Science and Technology at Illinois. "The brain circuits that underlie our ability to think-in this case to attend selectively to information in the environment-can change in a way that is conducive to better performance on tasks as a result of fitness." In simple terms, that means that walking at least 45 minutes a day boosts brain power as well as protecting your heart. An Herb for Menopause The physical changes that accompan> y menopause can be uncomfortable. But traditional herbal help is available: Black cohosh (Cimicifuga racemosa), an herb used for eons by aging women, has been shown in recent studies to be both safe and effective (Menopause 6/15/03). " This [research] should reassure health professionals that they can safely recommend black cohosh to their menopausal patients who cannot or choose not to take HRT [hormone replacement therapy]," says researcher Tieraona Low Dog, MD, Clinical Assistant Professor at the University of New Mexico Department of Family and Community Medicine. While HRT has been used to help women cope with menopause, a flurry of studies in the past few years have shown that HRT increases the risk of heart disease and cancer. Instead, black cohosh, which alleviates such menopausal discomforts as hot flashes, has been shown to be much safer. Keeping Track of Crucial Vitamins While continuing to take multivitamins and minerals at this age is important, some experts believe that as we grow older, vitamin D supplementation, as well as taking antioxidant nutrients, is particularly vital. Arthritis is a common affliction of aging, and rheumatoid arthritis (RA) is one particularly destructive form of this joint problem. But taking vitamin D can significantly lower your risk of this condition. When scientists analyzed the diets of 30,000 middle-aged women in Iowa over 11 years, they found that women who consumed vitamin D supplements were 34% less likely to suffer RA (Arth Rheu 1/03). Other vitamins are equally important to an older woman's well-being. For example, vitamins C and natural E have been found to lower the risk of stroke in those over the age of 55 (Neurology 11/11/03). In this study, smokers who consumed the most vitamin C and natural vitamin E were 70% were much less likely to suffer strokes than smokers whose diets were missing out on these vitamins. Rich sources of vitamin C in food include oranges and other citrus fruits, strawberries, red and green peppers, broccoli and brussels sprouts. Sources of vitamin E include vegetable oils such as sunflower seed, cottonseed, safflower, palm and wheat germ oils, margarine and nuts. Saving Your Sight After age 55, your eyes are particularly vulnerable. Eight million Americans of this age are at risk for age-related macular degeneration (AMD), a condition that destroys structures in the back of the eye necessary for vision (Arch Ophthal 11/03). But you can drop your risk of AMD by taking supplements of antioxidant vitamins and zinc, according to researchers at Johns Hopkins' Wilmer Eye Institute. Their research shows that a dietary supplement of vitamins C, natural vitamin E and beta carotene, along with zinc, lowers the chances of progressing to advanced AMD in certain at-risk people by about 25%. Daily supplements also reduced the risk of vision loss by about 19%. The carotenoids lutein and zeaxanthin also help protect aging eyes. When scientists compared healthy eyes with eyes suffering from AMD, they found that AMD eyes contained lower levels of these vital nutrients (Ophthalmology 2003; 109:1780). Furthermore, they found that levels of these chemicals generally decline as you grow older. Healthy at All Ages When it comes to designing a healthy lifestyle, general rules like these can be followed, but you should individualize your plan to fit your needs. No matter which type of exercises you pick out or what healthy foods you choose, look for a strategy and a plan you can stick to. If you think a selection of foods are good for you but you absolutely hate their taste, chances are you won't be able to stick to a diet that includes them. The same goes for exercise: Pick out activities that you enjoy and that you can perform consistently. That increases your chance of sticking to an exercise program. Staying healthy is enjoyable and it helps you get more out of life every day, no matter what stage of life you're in.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=335) Menopause: Disease or Condition?
Date:
June 13, 2005 03:44 PM
Menopause: Disease or Condition? by Mary Ann Mayo & Joseph L. Mayo, MD Energy Times, September 4, 1999 It's front-page news. It's politically correct and socially acceptable. Talking about menopause is in. Suddenly it's cool to have hot flashes. Millions of women turning 50 in the next few years have catapulted the subject of menopause into high-definition prominence. It's about time. Rarely discussed openly by women (what did your mother ever advise you?), meno-pause until recently was dismissed as "a shutting down experience characterized by hot flashes and the end of periods." Disparaging and depressing words like shrivel, atrophy, mood swings and melancholia peppered the scant scientific menopausal literature. What a difference a few years and a very vocal, informed and assertive group of Baby Boomers make. Staggered by the burgeoning numbers of newly confrontational women who will not accept a scribbled prescription and a pat on the head as adequate treatment, health practitioners and researchers have been challenged to unravel, explain and deal with the challenges of menopause. Not An Overnight Sensation Menopause, researchers have discovered, is no simple, clear cut event in a woman's life. The "change of life" does not occur overnight. A woman's body may begin the transition toward menopause in her early 40s, even though her last period typically occurs around age 51. This evolutionary time before the final egg is released is called the perimenopause. Erratic monthly hormone levels produce unexpected and sometimes annoying sensations. Even as their bodies adjust to lower levels of estrogen, progesterone and testosterone, some women don't experience typical signs of menopause until after the final period. A fortunate one-third have few or no discomforts. Hormonal Events According to What Your Doctor May Not Tell You About Premenopause (Warner Books) by John R. Lee, MD, Jesse Hanley, MD, and Virginia Hopkins, "The steroid hormones are intimately related to each other, each one being made from another or turned back into another depending on the needs of the body...But the hormones themselves are just part of the picture. It takes very specific combinations of vitamins, minerals and enzymes to cause the transformation of one hormone into another and then help the cell carry out the hormone's message. If you are deficient in one of the important hormone-transforming substances such as vitamin B6 or magnesium, for example, that too can throw your hormones out of balance. Thyroid and insulin problems, toxins, bad food and environmental factors, medication and liver function affect nutrient and hormone balance." The most important reproductive hormones include: Estrogen: the female hormone produced by the ovaries from puberty through menopause to regulate the menstrual cycle and prepare the uterus for pregnancy. Manufacture drops significantly during menopause. Estradiol is a chemically active and efficient form of estrogen that binds to many tissues including the uterus, breasts, ovaries, brain and heart through specific estrogen receptors that allow it to enter those cells, stimulating many chemical reactions. Estriol and estrone are additional forms of estrogen. Progesterone: also produced by the ovaries, it causes tissues to grow and thicken, particularly during pregnancy, when it protects and nurtures the fetus. Secretion ceases during menopause. Testosterone: Women produce about one-twentieth of what men do, but require it to support sex drive. About half of all women quit secreting testosterone during menopause. Estrogen's Wide Reach Since estrogen alone influences more than 400 actions on the body, chiefly stimulating cell growth, the effects of its fluctuations can be far-reaching and extremely varied: hot (and cold) flashes, erratic periods, dry skin (including the vaginal area), unpredictable moods, fuzzy thinking, forgetfulness, fatigue, low libido, insomnia and joint and muscle pain. Young women may experience premature menopause, which can occur gradually, as a matter of course, or abruptly with hysterectomy (even when the ovaries remain) or as a result of chemotherapy. Under such conditions symptoms can be severe. In the 1940s doctors reasoned that if most discomforts were caused by diminishing estrogen (its interactive role with progesterone and testosterone were underestimated), replacing it would provide relief. When unchecked estrogen use resulted in high rates of uterine cancer, physicians quickly began adding progesterone to their estrogen regimens and the problem appeared solved. For the average woman, however, hormone replacement therapy (HRT) became suspect and controversial, especially when a link appeared between extended use of HRT (from five to 10 years) and an increase in breast and endometrial cancers (Journal of Clinical Pharmacology 37, 1997). The result: Women have drawn a line in the sand between themselves and their doctors. Resolving The Impasse Since hormone replacement reduces the risk of major maladies like heart disease, osteoporosis, Alzheimer's, colon cancer and diabetes that would otherwise significantly rise as reproductive hormone levels decrease, most doctors recommend hormone replacement shortly before or as soon as periods stop. Hormone replacement also alleviates the discomforts of menopause. But only half of all women fill their HRT prescriptions and, of those who do, half quit within a year. Some are simply indifferent to their heightened medical risks. Some are indeed aware but remain unconvinced of the safety of HRT. Others complain of side effects such as bloating, headaches or drowsiness. Women's resistance to wholesale HRT has challenged researchers to provide more secure protection from the diseases to which they become vulnerable during menopause, as well as its discomforts. If the conventional medical practitioners do not hear exactly what modern women want, the complementary medicine community does. Turning to centuries-old botanicals, they have validated and compounded them with new technology. Their effectiveness depends on various factors including the synergistic interaction of several herbs, specific preparation, the correct plant part and dosage, harvesting and manufacturing techniques. Research demonstrates that plant hormones (phytoestrogens) protect against stronger potentially carcinogenic forms of estrogen while safely providing a hormone effect. Other herbs act more like tonics, zipping up the body's overall function. Help From Herbs Clinical trials and scientific processing techniques have resulted in plant-based supplements like soy and other botanicals that replicate the form and function of a woman's own estrogen. The complementary community also can take credit for pushing the conventional medical community to look beyond estrogen to progesterone in postmenopausal health. Natural soy or Mexican yam derived progesterone is formulated by pharmacologists in creams or gels that prevent estrogen-induced overgrowth of the uterine lining (a factor in uterine cancer), protect against heart disease and osteoporosis and reduce hot flashes (Fertility and Sterility 69, 1998: 96-101). A quarter of the women who take the popularly prescribed synthetic progesterone report increased tension, fatigue and anxiety; natural versions have fewer side effects. These "quasi-medicines," as Tori Hudson, a leading naturopathic doctor and professor at the National College of Naturopathic Medicine, Portland, Oregon, calls them, are considered "stronger than a botanical but weaker than a medicine." (Hudson is author of Gynecology and Naturopathic Medicine: A Treatment Manual.) According to Hudson, the amount of estrogen and progesterone in these supplements is much less than medical hormone replacement but equally efficacious in relieving menopausal problems and protecting the heart and bones. According to a study led by Harry K. Genant, PhD, of the University of California, San Francisco, "low-dose" plant estrogen derived from soy and yam, supplemented with calcium, prevents bone loss without such side effects as increased vaginal bleeding and endometrial hypoplasia, abnormal uterine cell growth that could be a precursor to endometrial cancer (Archives of Internal Medicine 157, 1997: 2609-2615). These herbal products, including natural progesterone and estrogen in the form of the weaker estriol or estrone, may block the effect of the stronger and potentially DNA-damaging estradiol. Soy in its myriad dietary and supplemental forms provides a rich source of isoflavones and phytosterols, both known to supply a mild estrogenic effect that can stimulate repair of the vaginal walls (Journal of the National Cancer Institute 83, 1991: 541-46). To enhance vaginal moisture, try the herb cimicifuga racemosa, the extract of black cohosh that, in capsule form, builds up vaginal mucosa (Therapeuticum 1, 1987: 23-31). Traditional Chinese herbal formulas containing roots of rehmannia and dong quai have long been reputed to promote vaginal moisture. Clinical research in Germany also confirms the usefulness of black cohosh in preventing hot flashes and sweating, as well as relieving nervousness, achiness and depressed moods caused by suppressed hormone levels. It works on the hypothalamus (the body's thermostat, appetite and blood pressure monitor), pituitary gland and estrogen receptors. Green tea is steeped with polyphenols, mainly flavonoids, that exert a massive antioxidant influence against allergens, viruses and carcinogens. The risks of estrogen-related cancers such as breast cancer are particularly lowered by these flavonoids, as these substances head directly to the breast's estrogen receptors. About three cups a day exert an impressive anti-inflammatory, antiallergenic, antiviral and anticarcinogenic effect. Other phytoestrogen-rich botanicals, according to Susun Weed's Menopausal Years: The Wise Woman Way (Ash Tree Publishing), include motherwort and lactobacillus acidophilus to combat vaginal dryness; hops and nettles for sleep disturbances; witch hazel and shepherd's purse for heavy bleeding; motherwort and chasteberry for mood swings; dandelion and red clover for hot flashes. Our Need For Supplements Adding micronutrients at Midlife to correct and counter a lifetime of poor diet and other habits is a step toward preventing the further development of the degenerative diseases to which we become vulnerable. At the very minimum, you should take: a multivitamin/mineral supplement vitamin E calcium Your multivitamin/mineral should contain vitamins A, B complex, C, D, E, calcium, magnesium, potassium, copper and zinc. Look for a wide variety of antioxidants that safeguard you from free radical damage, believed to promote heart disease and cancer, as well as contribute to the aging process. Also on the list: mixed carotenoids such as lycopene, alpha carotene and vitamin C; and folic acid to help regulate cell division and support the health of gums, red blood cells, the gastrointestinal tract and the immune system. Studies indicate a deficiency of folic acid (folate) in 30% of coronary heart disease, blood vessel disease and strokes; lack of folate is thought to be a serious risk factor for heart disease (OB.GYN News, July 15, 1997, page 28). Extra vitamin E is believed to protect against breast cancer and bolster immune strength in people 65 and older (Journal of the American Medical Association 277, 1997: 1380-86). It helps relieve vaginal dryness, breast cysts and thyroid problems and, more recently, hit the headlines as an aid in reducing the effects of Alzheimer's and heart disease. It is suspected to reduce the thickening of the carotid arterial walls and may prevent the oxidation of LDL (bad) cholesterol, which contributes to the formation of plaque in arteries. Selenium also has been identified as an assistant in halting cancer (JAMA 276, 1996: 1957-63). The Omegas To The Rescue Essential fatty acids found in cold water fish, flaxseed, primrose and borage oils and many nuts and seeds are essential for the body's production of prostaglandin, biochemicals which regulate hormone synthesis, and numerous physiological responses including muscle contraction, vascular dilation and the shedding of the uterine lining. They influence hormonal balance, reduce dryness and relieve hot flashes. In addition, the lignans in whole flaxseed behave like estrogen and act aggressively against breast cancer, according to rat and human studies at the University of Toronto (Nutr Cancer 26, 1996: 159-65). Research has demonstrated that these omega-3 and omega-6 fatty acids can reverse the cancer-causing effects of radiation and other carcinogens (Journal of the National Cancer Institute 74, 1985: 1145-50). Deficiencies may cause swelling, increased blood clotting, breast pain, hot flashes, uterine and menstrual cramps and constipation. Fatigue, lack of endurance dry skin and hair and frequent colds may signal EFA shortage. Plus, fatty fish oils, along with vitamin D and lactose, help absorption of calcium, so vital for maintaining bone mass. In addition, studies show that the natural substance Coenzyme A may help menopausal women reduce cholesterol and increase fat utilization (Med Hyp 1995; 44, 403, 405). Some researchers belive Coenzyme A plays a major role in helping women deal with stress while strengthening immunity. Still Suffering? Can't shake those menopausal woes? Menopause imposters may be imposing on you: The risk of thyroid disease, unrelenting stress, PMS, adrenal burnout, poor gastrointestinal health and hypoglycemia all increase at Midlife. Menopause is a handy hook on which to hang every misery, ache and pain but it may only mimic the distress of other ailments. For this reason every Midlife woman should have a good medical exam with appropriate tests to determine her baseline state of health. Only with proper analysis can you and your health practitioner hit on an accurate diagnosis and satisfying course of therapy. And if menopause is truly the issue, you have plenty of company. No woman escapes it. No woman dies from it. It is not a disease but a reminder that one-third of life remains to be lived. Menopausal Baby Boomers can anticipate tapping into creative energy apart from procreation. If not new careers, new interests await. An altered internal balance empowers a menopausal woman to direct, perhaps for the first time, her experience of life. She has come of age-yet again. Gone is the confusion, uncertainty, or dictates of a hormone driven life: This time wisdom and experience direct her. There is no need to yearn for youth or cower at the conventional covenant of old age. Menopause is the clarion call to reframe, reevaluate and reclaim. Mary Ann Mayo and Joseph L. Mayo, MD, are authors of The Menopause Manager (Revell) and executive editors of Health Opportunities for Women (HOW). Telephone number 877-547-5499 for more information.
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Date:
May 31, 2005 04:39 PM
Acetyl-L-carnitine is truly a mind-body nutrient. It helps synthesize acetylcholine, the brain's principal neurotransmitter responsible for learning and memory. And it is a more bioavailable form of L-carnitine, an amino acid derivative that performs the vital function of transporting longchain fatty acids into the cellular mitochondria where they are oxidized to generate metabolic energy. Supplemental acetyl-L-carnitine supports the activity of brain cells that depend on acetylcholine. It can also reduce the metabolic waste products that damage cells over time. As one of the most important nutrients to help slow the aging process, acetyl-L-carnitine is at the heart of Source Naturals' commitment to empower people to take charge of their own health. Acetylcholine is the brain's principal neurochemical of thought. Neurons need it to communicate with each other, especially to create and recall memories. Acetylcholine is also involved in muscular coordination. At neuromuscular junctions throughout the body, it tells muscles when to contract. But the efficiency of cells that use acetylcholine naturally declines with age, partly because of decreased activity of the enzyme that synthesizes this neurotransmitter. Neurotransmitter Production Acetylcholine is created when the enzyme choline acetyl transferase (CAT) attaches an acetyl group to a choline molecule. CAT activity is heightened by acetyl-L-carnitine, which donates its acetyl group. Acetyl-L-carnitine is made in small amounts naturally in the body, but its production begins to decline in Midlife. In well-controlled human studies, supplemental acetyl-L-carnitine slowed the progress of mental decline by notably improving attention and memory. When supplemental acetyl-L-carnitine was combined with lipoic acid (a powerful natural antioxidant), significant improvement in memory was seen in animals. Researchers said that together the two chemicals "tune up" the mitochondria, the energy-producing organelles that power all cells. Mitochondrial decay is believed to be the primary reason for age-related deterioration of cognitive function and energy levels. Cellular Energy and Protection As the active form of L-carnitine, acetyl L-carnitine efficiently transports long-chain fatty acids into the mitochondria where they are converted into ATP (adenosine triphosphate), the energy molecule. Animal studies suggest that supplemental acetyl L-carnitine has a positive effect on energy generation as well as on the structural integrity of aging mitochondria. By supporting fatty acid metabolism, acetyl L-carnitine also helps reduce lipofuscin, a metabolic waste product composed of damaged proteins and rancid fats. The brown "liver spots" on some elderly hands are composed of this aging pigment that gradually builds up in cells of the heart, liver, brain, and lens of the eye. Muscle Performance Ninety-five percent of the body's carnitine is found in muscle cells, especially in the heart where mitochondria comprise nearly 50% of a cell's volume. During prolonged exercise, muscles have a high demand for carnitine because fats can account for up to twothirds of the energy burned. L-carnitine supplements can increase exercise endurance and reduce fatigue. Acetyl L-carnitine is also a key nutrient in Source Naturals' legendary neuroceutical formulas MEGAMIND™ and HIGHER MIND™. And because acetyl L-carnitine also generates the basic energy that affects all biological and mental processes, this mind-body nutrient is one of the few nutritional compounds with such a broad range of action in maintaining youthful functioning. Source Naturals ACETYL L-CARNITINE is therefore an essential part of a smart strategy to live well, age well. References Carta A. and M. Calvani. Acetyl-L-carnitine: a drug able to slow the progress of Alzheimer's disease? Ann NY Acad Sci 1991; 640: 228-232. Hagen T.M. et al. August 4, 1998. Acetyl-L-carnitine fed to old rats partially restores mitochondrial function and ambulatory activity. Proc Natl Acad Sci USA 95(16):9562-6. Liu J. et al. February 19, 2002. Age-associated mitochondrial oxidative decay: Improvement of carnitine acetyltransferase substrate-binding affinity and activity in brain by feeding old rats acetyl-L-carnitine and/or R-alpha-lipoic acid. PNAS 99(4):1876-81. Spagnoli A.U. et al. 1991. Long-term acetyl-L-carnitine treatment in Alzheimer’s disease. Neurology. 41(11):1726-1732.
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