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fitspresso

https://www.thefastleanpro.us/ - 0 views

www.thefastleanpro.us

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shared by fitspresso on 27 Sep 23 - No Cached
  • fitspresso on 27 Sep 23
     
    Fast Lean Pro™ (official) | weight lose Formula thefastleanpro.us · by Fast Lean Pro Fast Lean Pro Only $49/Bottle Limited Time Offer! Fast Lean Pro Special Deal + Special 51% Discount Save $300 + 180 Days Money Back Guarantee FastLeanPro The #1 Solution To natural metabolism booster helps you lose weight quickly without starving yourself. Fast Lean Pro is a natural powder supplement for weight loss that has recently been developed by Japanese scientists. Regular Price: $99/per bottle Only for: $49/per bottle What Is Fast Lean Pro? Fast Lean Pro is a powdered dietary powdery supplement designed to aid in weight loss. It contains a unique combination of ingredients that are believed to activate the body's "fasting switch" to optimize results. This product focuses not only on weight loss but also on promoting cellular rejuvenation, fasting, and a healthy metabolism. The concept behind Fast Lean Pro is that incorporating fasting into one's lifestyle can lead to positive outcomes irrespective of individual food choices and eating habits. To comprehend the mechanism of the Fast Lean Pro process, it is necessary to delve into its specific details. One of the few weight loss pills on the market that contains Fibersol is Fast Lean Pro. This safe, specialized fiber adds bulk to its weight when combined with water, curbing your appetite before it throws off your meal plan. If you're trying to lose weight or curb your appetite, Fast Lean Pro can help. Supporting substances such as niacin and chromium contribute to this. The body can further benefit from these nutrients, such as through improved metabolic regulation. Fast lean Pro is non-GMO, vegan friendly, and contains no artificial ingredients or stimulants. Fast Lean Pro is a weight loss product that promotes the body's natural self-feeding process. The body naturally removes old, damaged cells through a process known as autophagy to encourage cell regeneration and repair. Recent studies by a group
Nathan Goodyear

Access : The neurobiology of appetite: hunger as addiction : International Journal of O... - 0 views

www.nature.com/...ijo200969a.html

overweight obesity over-eating hunger addiction

shared by Nathan Goodyear on 19 Mar 12 - No Cached
  • Nathan Goodyear on 19 Mar 12
     
    complex interplay between behavior, genetics, and CNS play role in over-eating.  Add in environment as well.
Nathan Goodyear

A role for ghrelin in the central regulation of feeding : Abstract : Nature - 0 views

www.nature.com/...409194A0.html

ghrelin weight overweight obesity IR insulin resistance over-eating

shared by Nathan Goodyear on 21 Nov 11 - No Cached
  • Nathan Goodyear on 21 Nov 11
     
    ghrelin plays central role in positive energy balance.  Ghrelin is produced from stomach to increase appetite prior to eating and then decreases post meal to provide satiety.  In some, the post meal ghrelin remains elevated and thus overeating ensues.  Important point, is that low ghrelin has been shown to lead to insulin resistance.
Nathan Goodyear

Pleasure Eating Triggers Body's Reward System and May Stimulate Overeating - 0 views

www.endo-society.org/...d-May-Stimulate-Overeating.cfm

Ghrelin overeating obesity overweight appetite

shared by Nathan Goodyear on 27 Jun 12 - No Cached
  • Nathan Goodyear on 27 Jun 12
     
    Ghrelin plays a role in overeating.  This is not much of a surprise as Ghrelin has been shown to be a major appetite driver and has been linked to higher calorie intake of foods.
Nathan Goodyear

The gut-liver-axis: Endotoxemia, inflammation, insulin resistance and NASH - 0 views

www.journal-of-hepatology.eu/...abstract

metabolic endotoxemia obesity overweight LPS bifidobacterium inflammaiton gut insulin resistance

shared by Nathan Goodyear on 20 Jan 12 - No Cached
  • Nathan Goodyear on 20 Jan 12
     
    metabolic endotoxemia starts with what you eat.  Chronic over nutrition results in elevated LPS. This starts a cascade of events that results in inflammation.  A well balanced gut flora of bifidobacterium is one way to slow this trigger.
Nathan Goodyear

Brain dopamine and obesity : The Lancet - 0 views

www.thelancet.com/...fulltext

dopamine BMI obesity overweight

shared by Nathan Goodyear on 27 Feb 12 - No Cached
  • Nathan Goodyear on 27 Feb 12
     
    Dopamine found to be inversely associated with BMI.  The higher the BMI, the lower the dopamine levels.  This low dopamine would result in a proposed "pathological eating".  As dopamine is the "pleasure" neurotransmitter, it would be easy to see how low dopamine would result in overeating.
Nathan Goodyear

Foods fail to suppress Ghrelin levels in obese humans - 0 views

jcem.endojournals.org/...2984.full.pdf+html

gherlin obesity overweight weight-loss hormone

shared by Nathan Goodyear on 08 Mar 12 - No Cached
  • Nathan Goodyear on 08 Mar 12
     
    Ghrelin is a hormone that is release to induce hunger and eating. Post meals, gherlin should decrease; but in obese individuals, a dysregulation between the GI system and the hypothalamus results in elevated gherlin resulting in overeating.
fnfdoc

Habits That Ruin Your Weight Loss Plan | Health Blog - 0 views

fnfdoc.com/...its-ruin-your-weight-loss-plan

Weight Loss Plan Habits Diet Binge Eating

shared by fnfdoc on 19 Sep 18 - No Cached
  • fnfdoc on 19 Sep 18
     
    Some Habits That Ruin Your Weight Loss Plan. Although we may follow a strict diet plan and hit the gym.., sometimes it becomes nearly impossible to get rid of those extra pounds... The problem lies with the seemingly harmless everyday habits that we have nurtured over the years and...
  • fnfdoc on 19 Sep 18
     
    While most of us are aware that eating cheesy sausages every day for breakfast is not really good for the waistline, there are many other subtle bad habits that keep on adding more pounds to our bodies. These habits are harmful because they have the potential to sabotage our weight loss plan.
fitspresso

https://www.sightcare-co.com/ - 0 views

www.sightcare-co.com

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shared by fitspresso on 27 Sep 23 - No Cached
  • fitspresso on 27 Sep 23
     
    Sight Care | Official Site sightcare-co.com · by Sight Care Sight Care Only $49/Bottle Limited Time Offer! Sight Care Special Deal + Special 67% Discount Save $600 + 180 Days Money Back Guarantee #1.The Sight Care vision supplement is a dietary supplement for helping you improve your vision and brain health. Sight Care eye supplements are formulated to provide a synergistic blend of vitamins, minerals, antioxidants, and other bioactive compounds that are essential for maintaining healthy vision Regular Price: 147/per bottle Only for: $49/per bottle What Is Sight Care? This powerful vision support supplement is made with a unique blend of natural ingredients and plant extracts that work together synergistically to deliver numerous benefits for your brain and eye health. With Sight Care, you can expect to experience increased energy levels, improved eyesight, and an overall revitalized sense of well-being. Taking care of your vision health is not just about seeing clearly; it's also about maintaining your overall brain health. As we age, our vision deteriorates, and our eyes and brain can experience a decline in function, but there are steps you can take to support your visual and cognitive health. Regular eye exams are crucial for detecting and treating vision problems early on, and making healthy choices such as eating a nutritious diet and exercising regularly can also help. However, with busy schedules, it can be difficult to find the time to devote to a healthy lifestyle. This is where the Sight Care supplement comes in. It's designed to support both vision and brain health with its blend of natural ingredients that have been shown to promote healthy vision and cognitive function You must not compromise your eye health for momentary exhilaration. If you are glued to digital screens day and night, you must take measures to prevent eye diseases like age-related macular degeneration. The SightCare vision supplement has been made using 100% natura
Nathan Goodyear

Inflammatory cause of metabolic syndrome via brain stress and NF-κB - 0 views

www.ncbi.nlm.nih.gov/...PMC3314172

metabolic syndrome TLR cytokines hypothalamus brain neurology metabolic syndrome NF-kappaB DIO diet induced obesity over nutrition nutrition inflammation

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Mechanistic studies further showed that such metabolic inflammation is related to the induction of various intracellular stresses such as mitochondrial oxidative stress, endoplasmic reticulum (ER) stress, and autophagy defect under prolonged nutritional excess
  • intracellular stress-inflammation process for metabolic syndrome has been established in the central nervous system (CNS) and particularly in the hypothalamus
  • the CNS and the comprised hypothalamus are known to govern various metabolic activities of the body including appetite control, energy expenditure, carbohydrate and lipid metabolism, and blood pressure homeostasis
  • ...56 more annotations...
  • Reactive oxygen species (ROS) refer to a class of radical or non-radical oxygen-containing molecules that have high oxidative reactivity with lipids, proteins, and nucleic acids
  • a large measure of intracellular ROS comes from the leakage of mitochondrial electron transport chain (ETC)
  • Another major source of intracellular ROS is the intentional generation of superoxides by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase
  • there are other ROS-producing enzymes such as cyclooxygenases, lipoxygenases, xanthine oxidase, and cytochrome p450 enzymes, which are involved with specific metabolic processes
  • To counteract the toxic effects of molecular oxidation by ROS, cells are equipped with a battery of antioxidant enzymes such as superoxide dismutases, catalase, peroxiredoxins, sulfiredoxin, and aldehyde dehydrogenases
  • intracellular oxidative stress has been indicated to contribute to metabolic syndrome and related diseases, including T2D [72; 73], CVDs [74-76], neurodegenerative diseases [69; 77-80], and cancers
  • intracellular oxidative stress is highly associated with the development of neurodegenerative diseases [69] and brain aging
  • dietary obesity was found to induce NADPH oxidase-associated oxidative stress in rat brain
  • mitochondrial dysfunction in hypothalamic proopiomelanocortin (POMC) neurons causes central glucose sensing impairment
  • Endoplasmic reticulum (ER) is the cellular organelle responsible for protein synthesis, maturation, and trafficking to secretory pathways
  • unfolded protein response (UPR) machinery
  • ER stress has been associated to obesity, insulin resistance, T2D, CVDs, cancers, and neurodegenerative diseases
  • brain ER stress underlies neurodegenerative diseases
  • under environmental stress such as nutrient deprivation or hypoxia, autophagy is strongly induced to breakdown macromolecules into reusable amino acids and fatty acids for survival
  • intact autophagy function is required for the hypothalamus to properly control metabolic and energy homeostasis, while hypothalamic autophagy defect leads to the development of metabolic syndrome such as obesity and insulin resistance
  • prolonged oxidative stress or ER stress has been shown to impair autophagy function in disease milieu of cancer or aging
  • TLRs are an important class of membrane-bound pattern recognition receptors in classical innate immune defense
  • Most hypothalamic cell types including neurons and glia cells express TLRs
  • overnutrition constitutes an environmental stimulus that can activate TLR pathways to mediate the development of metabolic syndrome related disorders such as obesity, insulin resistance, T2D, and atherosclerotic CVDs
  • Isoforms TLR1, 2, 4, and 6 may be particularly pertinent to pathogenic signaling induced by lipid overnutrition
  • hypothalamic TLR4 and downstream inflammatory signaling are activated in response to central lipid excess via direct intra-brain lipid administration or HFD-feeding
  • overnutrition-induced metabolic derangements such as central leptin resistance, systemic insulin resistance, and weight gain
  • these evidences based on brain TLR signaling further support the notion that CNS is the primary site for overnutrition to cause the development of metabolic syndrome.
  • circulating cytokines can limitedly travel to the hypothalamus through the leaky blood-brain barrier around the mediobasal hypothalamus to activate hypothalamic cytokine receptors
  • significant evidences have been recently documented demonstrating the role of cytokine receptor pathways in the development of metabolic syndrome components
  • entral administration of TNF-α at low doses faithfully replicated the effects of central metabolic inflammation in enhancing eating, decreasing energy expenditure [158;159], and causing obesity-related hypertension
  • Resistin, an adipocyte-derived proinflammatory cytokine, has been found to promote hepatic insulin resistance through its central actions
  • both TLR pathways and cytokine receptor pathways are involved in central inflammatory mechanism of metabolic syndrome and related diseases.
  • In quiescent state, NF-κB resides in the cytoplasm in an inactive form due to inhibitory binding by IκBα protein
  • IKKβ activation via receptor-mediated pathway, leading to IκBα phosphorylation and degradation and subsequent release of NF-κB activity
  • Research in the past decade has found that activation of IKKβ/NF-κB proinflammatory pathway in metabolic tissues is a prominent feature of various metabolic disorders related to overnutrition
  • it happens in metabolic tissues, it is mainly associated with overnutrition-induced metabolic derangements, and most importantly, it is relatively low-grade and chronic
  • this paradigm of IKKβ/NF-κB-mediated metabolic inflammation has been identified in the CNS – particularly the comprised hypothalamus, which primarily accounts for to the development of overnutrition-induced metabolic syndrome and related disorders such as obesity, insulin resistance, T2D, and obesity-related hypertension
  • evidences have pointed to intracellular oxidative stress and mitochondrial dysfunction as upstream events that mediate hypothalamic NF-κB activation in a receptor-independent manner under overnutrition
  • In the context of metabolic syndrome, oxidative stress-related NF-κB activation in metabolic tissues or vascular systems has been implicated in a broad range of metabolic syndrome-related diseases, such as diabetes, atherosclerosis, cardiac infarct, stroke, cancer, and aging
  • intracellular oxidative stress seems to be a likely pathogenic link that bridges overnutrition with NF-κB activation leading to central metabolic dysregulation
  • overnutrition is an environmental inducer for intracellular oxidative stress regardless of tissues involved
  • excessive nutrients, when transported into cells, directly increase mitochondrial oxidative workload, which causes increased production of ROS by mitochondrial ETC
  • oxidative stress has been shown to activate NF-κB pathway in neurons or glial cells in several types of metabolic syndrome-related neural diseases, such as stroke [185], neurodegenerative diseases [186-188], and brain aging
  • central nutrient excess (e.g., glucose or lipids) has been shown to activate NF-κB in the hypothalamus [34-37] to account for overnutrition-induced central metabolic dysregulations
  • overnutrition can present the cell with a metabolic overload that exceeds the physiological adaptive range of UPR, resulting in the development of ER stress and systemic metabolic disorders
  • chronic ER stress in peripheral metabolic tissues such as adipocytes, liver, muscle, and pancreatic cells is a salient feature of overnutrition-related diseases
  • recent literature supports a model that brain ER stress and NF-κB activation reciprocally promote each other in the development of central metabolic dysregulations
  • when intracellular stresses remain unresolved, prolonged autophagy upregulation progresses into autophagy defect
  • autophagy defect can induce NF-κB-mediated inflammation in association with the development of cancer or inflammatory diseases (e.g., Crohn's disease)
  • The connection between autophagy defect and proinflammatory activation of NF-κB pathway can also be inferred in metabolic syndrome, since both autophagy defect [126-133;200] and NF-κB activation [20-33] are implicated in the development of overnutrition-related metabolic diseases
  • Both TLR pathway and cytokine receptor pathways are closely related to IKKβ/NF-κB signaling in the central pathogenesis of metabolic syndrome
  • Overnutrition, especially in the form of HFD feeding, was shown to activate TLR4 signaling and downstream IKKβ/NF-κB pathway
  • TLR4 activation leads to MyD88-dependent NF-κB activation in early phase and MyD88-indepdnent MAPK/JNK pathway in late phase
  • these studies point to NF-κB as an immediate signaling effector for TLR4 activation in central inflammatory response
  • TLR4 activation has been shown to induce intracellular ER stress to indirectly cause metabolic inflammation in the hypothalamus
  • central TLR4-NF-κB pathway may represent one of the early receptor-mediated events in overnutrition-induced central inflammation.
  • cytokines and their receptors are both upstream activating components and downstream transcriptional targets of NF-κB activation
  • central administration of TNF-α at low dose can mimic the effect of obesity-related inflammatory milieu to activate IKKβ/NF-κB proinflammatory pathways, furthering the development of overeating, energy expenditure decrease, and weight gain
  • the physiological effects of IKKβ/NF-κB activation seem to be cell type-dependent, i.e., IKKβ/NF-κB activation in hypothalamic agouti-related protein (AGRP) neurons primarily leads to the development of energy imbalance and obesity [34]; while in hypothalamic POMC neurons, it primarily results in the development of hypertension and glucose intolerance
  • the hypothalamus, is the central regulator of energy and body weight balance [
  • Nathan Goodyear on 09 Jul 13
     
    Great article chronicles the biochemistry of "over nutrition" and inflammation through NF-kappaB activation and its impact on the brain.
Nathan Goodyear

Effects of short-term high-fat overfeeding on genome-wide DNA methylation in the skelet... - 0 views

link.springer.com/...10.1007%2Fs00125-012-2717-8

epigenetics methylation nutrition high fat diet

shared by Nathan Goodyear on 03 Oct 17 - No Cached
  • short-term HFO introduces DNA methylation changes on a genome-wide scale in human skeletal muscle
  • These changes were only partly reversed after 6–8 weeks
  • The induction of DNA methylation changes after 5 days of HFO supports the growing awareness of DNA methylation as a dynamic signal that is possibly relevant to short-term day-to-day metabolic adaptations, including acute exercise
  • ...4 more annotations...
  • Diverging DNA methylation levels between elderly, but not young, genetically identical twins indicate that environmental exposures throughout life may permanently influence DNA methylation, suggesting some preservation of de novo DNA methylation in adults
  • our finding of a slow reversibility rate indicates the demethylation process may be somewhat impeded compared with the induction of methylation changes by diet, which could have implications for the preservation or build-up of CpG methylation over time
  • A slow reversibility of DNA methylation induced by carcinogenic agents has likewise been observed due to ingestion of high-fat diets in rodents
  • the relationship between DNA methylation and gene expression is not always straightforward
  • Nathan Goodyear on 03 Oct 17
     
    Study finds variability of methylation and some genetic expression alteration with high fat diet.  Restated, what you eat interacts with your DNA to alter genetic expression.  This has implications on initiation of therapy as well as response to therapy.
Nathan Goodyear

Brain dopamine transporters in obesity -- Yao et al. 51 (1002): 1820 -- Society of Nucl... - 0 views

jnumedmtg.snmjournals.org/...1820

dopamine transporters obesity receptors brain

shared by Nathan Goodyear on 29 Apr 11 - No Cached
  • The dopaminergic deficiency mechanism in obesity may primarily involve in dopamine receptors, but not dopamine transporters in a subset of non-binge eating obesity
  • Nathan Goodyear on 29 Apr 11
     
    Dopamine transporters don't appear to have role in overeating and obesity; more likely involves dopamine receptors
pharmacybiz

NHS New Campaign To Promote Better Care For Mental Health - 0 views

www.pharmacy.biz/-better-care-for-mental-health

NHS-Better-Health-campaign pharmacy-business NHS-Better-Health-app NHS-healthy-eating NHS-Better-Health-lose-weight NHS-Better-health-every-Mind-matters

shared by pharmacybiz on 18 Jan 22 - No Cached
  • pharmacybiz on 18 Jan 22
     
    The NHS is going to launch a new campaign using the iconic Beatles song 'Help!" to encourage people to take better care of their mental health. The campaign, being launched today (January 17), is backed by some of the UK's biggest artists, urging people to seek support for their mental wellbeing. Since the beginning of the pandemic around 2.3 million people have come forward for NHS talking therapies, with over 50 per cent being concerned about their mental health last year. The NHS is encouraging anybody experiencing anxiety, depression, or other common mental health concerns to experience how talking therapies can help them. NHS mental health talking therapies are a confidential service run by fully trainedexperts that can be accessed through self-referral or GP practice.
Nathan Goodyear

Central Nervous system control of food intake - 0 views

www.saegre.org.ar/...schwartz_2000.pdf

CNS gut eating overeating obesity overweight weight-loss leptin insulin ghrelin adiponectin

shared by Nathan Goodyear on 28 Feb 12 - No Cached
  • Nathan Goodyear on 28 Feb 12
     
    For you biochemistry junkies. A great review of how the Gut and CNS communicate to regulate food intake
wheelchairindia9

Folding Wheelchair - 0 views

www.wheelchairindia.com/...Folding-Wheelchair

Lightweight Folding Recline Wheelchairs portable and compact shape folding wheelchair lighter and easier to lift maximum comfort and health reclining wheelchair

shared by wheelchairindia9 on 11 May 15 - No Cached
  • wheelchairindia9 on 11 May 15
     
    Lightweight, compact-folding wheelchairs for children, teenagers, and young adults let go anywhere, while still ensuring proper positioning and support. Going to school, appointments and even on vacation is possible with the convenient, lightweight design. Just fold it up and put it in trunk. Foldable Wheelchair by features a powder coat steel frame with durable nylon upholstery and padded armrests. Composite mag wheels with maintenance-free bearings and composite handrims make for a smooth ride. As with anything with moveable parts, the folding wheelchair is not as durable as the rigid frame wheelchair. Therefore maintenance is required more frequently to keep all parts in good working order. Before purchasing a wheelchair, consider all activity level. If traveling often, and need a highly-portable option, a folding lightweight wheelchair may be. Lightweight wheelchairs provide convenience and comfort to the user and caregiver alike and are often built using materials like aluminum and titanium alloy, while foldable wheelchairs allow for easy storage and transport. Merge the two styles, and got a great mobility aid that isn't a pain to lug around. Folding wheelchairs also have removable foot rests which allow for easy folding. Most frames are made from aluminum or titanium and are heavier than the rigid frame. wheelchair is designed to fit the body of the user, while the primary design of the folding wheelchair is to fold. Folding wheelchairs are generally more "boxy" while rigid wheelchairs conform to the shape of the body. This means it can hold the users body in place by tapering the frame and seat. The folding wheelchair cannot be tapered or it would not close completely. Features: Powder coat steel frame. Durable nylon upholstery. Composite mag wheels with maintenance-free bearings. Composite footplates. Padded armrests. Composite handrims. Maximum weight capacity.
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