Tag: longevity

TREATMENT OF AGE-RELATED AND MITOCHONDRIAL DISEASES BY INHIBITION OF HIF-1 ALPHA FUNCTION – President and Fellows of Harvard College

TREATMENT OF AGE-RELATED AND MITOCHONDRIAL DISEASES BY INHIBITION OF HIF-1 ALPHA FUNCTION – President and Fellows of Harvard College

Following we have a new patent application from Dr. David Sinclair et al

It describes the use of NMN on humans and dosage rates.

https://www.freepatentsonline.com/y2020/0291100.html

Effects of oily fish intake on cognitive and socioemotional function in healthy 8–9-year-old children: the FiSK Junior randomized trial | The American Journal of Clinical Nutrition | Oxford Academic

Effects of oily fish intake on cognitive and socioemotional function in healthy 8–9-year-old children: the FiSK Junior randomized trial | The American Journal of Clinical Nutrition | Oxford Academic

Oily fish dose-dependently improved cognitive function, especially attention and cognitive flexibility, and reduced socioemotional problems. The results support the importance of n–3 LCPUFAs for optimal brain function and fish intake recommendations in children.

https://academic.oup.com/ajcn/article/112/1/74/5855515?searchresult=1

Effects of oily fish intake on cognitive and socioemotional function in healthy 8–9-year-old children: the FiSK Junior randomized trial | The American Journal of Clinical Nutrition | Oxford Academic

Effects of oily fish intake on cognitive and socioemotional function in healthy 8–9-year-old children: the FiSK Junior randomized trial | The American Journal of Clinical Nutrition | Oxford Academic

Oily fish dose-dependently improved cognitive function, especially attention and cognitive flexibility, and reduced socioemotional problems. The results support the importance of n–3 LCPUFAs for optimal brain function and fish intake recommendations in children.

https://academic.oup.com/ajcn/article/112/1/74/5855515?searchresult=1

Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations | JACC: Journal of the American College of Cardiology

Dave Asprey seems to do a good job at explaining what this study means:

“Something truly epic happened today that is going to change what you eat for years to come. Truly epic. The Journal of the American College of cardiology published a groundbreaking paper today admitting something that you already knew if you had been on the Bulletproof Diet for the last 10 years. (Yes, I am feeling slightly vindicated after receiving so much resistance after writing The Bulletproof Diet, which eventually helped people lose about 1,000,000 pounds!)This new paper, which uses data from studying 135,000 people overtime, finds:-Saturated fat from meat and dairy do not cause an increase in cardiovascular disease, and reduce stroke risk.-Polyunsaturated fats increase risk of cardiovascular disease.-Different fats do different things-Cutting saturated fat does not reduce death rate-the 25% of people eating the highest saturated fat intake (about ∼14% of calories) had lower risk of stroke-Only 5% of fat should be polyunsaturated for lowest death. This is effectively a deathblow to vegan and plant-based practices, which make people sick over time because they contain almost all polyunsaturated fats. It’s one reason I got sicker when I was a vegan. (It takes 2 years to replace half your cell membrane fats when you change your diet.)”

Niacin Increases NAD+ Significantly in Human Trial | Lifespan.io

Niacin Increases NAD+ Significantly in Human Trial | Lifespan.io

The results of a new human trial using niacin shed new light on its role in NAD+ biology [1].

The trial participants were given a steadily increasing dose of niacin, starting at 250 mg/day to 750-1000 mg/day over a 4-month period, then a 10-month follow-up treatment period. The participants were organized into a study group of individuals with mitochondrial myopathy and a control group of healthy age-matched people consisting of two healthy people for each patient with mitochondrial myopathy. All the study participants were placed on the same niacin supplementation regimen.

The researchers report that niacin treatment increased muscle NAD+ levels by 1.3-fold at 4 months and 2.3-fold after 10 months in the study group.

https://www.lifespan.io/news/niacin-increases-nad-significantly-in-human-trial/

Niacin Increases NAD+ Significantly in Human Trial | Lifespan.io

Niacin Increases NAD+ Significantly in Human Trial | Lifespan.io

The results of a new human trial using niacin shed new light on its role in NAD+ biology [1].

The trial participants were given a steadily increasing dose of niacin, starting at 250 mg/day to 750-1000 mg/day over a 4-month period, then a 10-month follow-up treatment period. The participants were organized into a study group of individuals with mitochondrial myopathy and a control group of healthy age-matched people consisting of two healthy people for each patient with mitochondrial myopathy. All the study participants were placed on the same niacin supplementation regimen.

The researchers report that niacin treatment increased muscle NAD+ levels by 1.3-fold at 4 months and 2.3-fold after 10 months in the study group.

https://www.lifespan.io/news/niacin-increases-nad-significantly-in-human-trial/

Niacin Increases NAD+ Significantly in Human Trial | Lifespan.io

Niacin Increases NAD+ Significantly in Human Trial | Lifespan.io

The results of a new human trial using niacin shed new light on its role in NAD+ biology [1].

The trial participants were given a steadily increasing dose of niacin, starting at 250 mg/day to 750-1000 mg/day over a 4-month period, then a 10-month follow-up treatment period. The participants were organized into a study group of individuals with mitochondrial myopathy and a control group of healthy age-matched people consisting of two healthy people for each patient with mitochondrial myopathy. All the study participants were placed on the same niacin supplementation regimen.

The researchers report that niacin treatment increased muscle NAD+ levels by 1.3-fold at 4 months and 2.3-fold after 10 months in the study group.

https://www.lifespan.io/news/niacin-increases-nad-significantly-in-human-trial/

Australian-made wearable biosensors to gather precision data on chronic disease – Hardware – iTnews

Australian-made wearable biosensors to gather precision data on chronic disease – Hardware – iTnews

Melbourne-based company Nutromics is developing the alternative to painful finger pricks and blood tests to measure key dietary biomarkers in real time.

Australian-made wearable biosensors to gather precision data on chronic disease – Hardware – iTnews

Consumer trends during Covid-19

Some interesting and somewhat encouraging news from the Woolworths CEO today via his email updates during Covid-19 show some interesting trends in consumer spending on food and vitamins during this time.

To quote from his email:

We are becoming healthier and more adventurous in our cooking
While the slow cooking movement continues, we’re also becoming increasingly adventurous. Ingredients such as cardamom, saffron and dried sesame seeds have doubled in sales. Roasted peppers are up 65%, Asian and hot chilli sauces are both up 40% and capers are up 35%.

We’re also well into soup season. What’s interesting this year is the explosive growth of dried soup mix packets (up 200%) as people make more warming soup at home.

It’s also interesting to see customers think about their health, with a big rise in vitamin sales, plus ground ginger and turmeric sales up 120% and sauerkraut up 76%. On a related topic, sales of cough and cold products are much lower this year compared to last year.”

This is encouraging and hopefully a sign that the general population is starting to become more interested in preparing fresh meals rather than fast food, and hopefully the rise in vitamins and other beneficial products is a sign that people are starting to see value in improving their health and eating better.

It’s pretty clear that the more fit and healthy you are and the better you eat, the less likely you are to contract Covid-19 and, less likely to have severe complication if you do. We have been keeping an eye on developments and have been hoping that the silver lining from all of this may be a new focus on health and well-being.

So please ensure you take some time out of your busy life to focus on whats really important, your life! We at Health Hacker wish all of you good health and encourage you to keep exploring and trying to improve your diet and lifestyle as much as possoble. Remember, something is better than nothing so start on somethign today!

Part 1: My COVID-19 update – April 1st – Dr David A Sinclair

“It’s April 1st, 2020. If only the headlines were a joke. Our nation’s leaders will soon be faced with a difficult choice. Hunker down for another four months and wreck the economy or let people out in two months and kill an additional hundred thousand people.

Professor Samir Bhatt, Senior Lecturer at the Imperial College of London, and his colleagues calculate that, globally, up to 43 million people have been infected with SARS-CoV-2. They predict that if we’d gone about our normal lives, COVID-19 would have caused 7 billion infections and 40 million deaths this year. Shielding only the elderly may have halved the number of deaths, a strategy the UK initially entertained, but health systems would have been overwhelmed, so that tactic was largely abandoned.

Based on the advice of professional epidemiologists, most nations have adopted a stretch-it-out and hope it doesn’t return strategy. It seems to be working so far. Rates of new cases are declining in Europe and the US. If the current suppression strategies are sustained, then 38.7 million lives globally will be saved this year, the epidemiologists at the Imperial College calculate. 

But epidemiologists aren’t economists. We can not stay home for the rest of the year – the economic impact would be too high. We are three weeks into the shutdown and already factories are ceasing production, brick-and-mortar retail stores and restaurants are closed, unemployment spikes are unprecedented, commodity prices have plunged, and a wave of loan defaults is expected.

A colleague on a global pandemic response panel tells me the panel’s best estimate is that the US economy will rebound rapidly, but only if the nation returns to work in 60 days. After that, it’s anyone’s guess. No one, not even the experts, are willing to estimate the full economic impact of COVID-19. It will depend on how long it takes to get back to work and how many times we will be sent back home.”

https://mailchi.mp/lifespanbook.com/my-covid-19-update-2572786

Estimating clinical severity of COVID-19 from the transmission dynamics in Wuhan, China | Nature Medicine

Estimating clinical severity of COVID-19 from the transmission dynamics in Wuhan, China | Nature Medicine

As of 29 February 2020 there were 79,394 confirmed cases and 2,838 deaths from COVID-19 in mainland China. Of these, 48,557 cases and 2,169 deaths occurred in the epicenter, Wuhan. A key public health priority during the emergence of a novel pathogen is estimating clinical severity, which requires properly adjusting for the case ascertainment rate and the delay between symptoms onset and death. Using public and published information, we estimate that the overall symptomatic case fatality risk (the probability of dying after developing symptoms) of COVID-19 in Wuhan was 1.4% (0.9–2.1%), which is substantially lower than both the corresponding crude or naïve confirmed case fatality risk (2,169/48,557 = 4.5%) and the approximator1 of deaths/deaths + recoveries (2,169/2,169 + 17,572 = 11%) as of 29 February 2020. Compared to those aged 30–59 years, those aged below 30 and above 59 years were 0.6 (0.3–1.1) and 5.1 (4.2–6.1) times more likely to die after developing symptoms. The risk of symptomatic infection increased with age (for example, at ~4% per year among adults aged 30–60 years).

https://www.nature.com/articles/s41591-020-0822-7?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Dietary Intakes of Minerals, Essential and Toxic Trace Elements for Adults from Eragrostis tef L.: A Nutritional Assessment

Dietary Intakes of Minerals, Essential and Toxic Trace Elements for Adults from Eragrostis tef L.: A Nutritional Assessment

“This study analysed the contents of thirty-six mineral and trace elements in teff (Eragrostis tef L.) grains. What is more, dietary intakes were calculated. Inductively coupled plasma mass spectrometry (ICP-MS) was used to assess mineral and trace element contents. Consequently, the appropriate Recommended Dietary Allowance (RDA) or adequate intake (AI), and provisional tolerable weekly intake (PTWI) or provisional tolerable monthly intake (PTMI) values for adults were determined according to the Food and Agriculture Organization/World Health Organization (FAO/WHO) and Institute of Medicine (IOM) regulations. Teff is a significant contributor to RDAs and AIs for females in the following order: Mn > Cu > Zn ≥ Mg > Fe ≥ P and Ca. For males, teff contributes in the order, Mn > Cu > Fe > Zn ≥ P ≥ Mg > and Ca. The concentration of arsenic (65.9 µg/kg) in brown teff originating in Bolivia exceeded the average acceptable value set by Reg. No. 1881 of 6–50 µg/kg in cereals consumed in the EU. The PTWIs or PTMIs for Al, Cd, Sn and Hg were all under 7%, which is below the limits of toxic element intake related to the body weight of 65 kg for adult females and 80 kg for males, set by the FAO/WHO. Teff grains can be recommended as a valuable and safe source of minerals and trace elements.”

Nutrients | Free Full-Text | Dietary Intakes of Minerals, Essential and Toxic Trace Elements for Adults from Eragrostis tef L.: A Nutritional Assessment | HTML
Metabolic Effects of Intermittent Fasting | Annual Review of Nutrition

Metabolic Effects of Intermittent Fasting | Annual Review of Nutrition

“Intermittent fasting regimens are hypothesized to influence metabolic regulation via effects on (a) circadian biology, (b) the gut microbiome, and (c) modifiable lifestyle behaviors, such as sleep. If proven to be efficacious, these eating regimens offer promising nonpharmacological approaches to improving health at the population level, with multiple public health benefits.”

https://www.annualreviews.org/doi/abs/10.1146/annurev-nutr-071816-064634?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

The Neuroprotective Properties of Hericium erinaceus in Glutamate-Damaged Differentiated PC12 Cells and an Alzheimer’s Disease Mouse Model

The Neuroprotective Properties of Hericium erinaceus in Glutamate-Damaged Differentiated PC12 Cells and an Alzheimer’s Disease Mouse Model

Hericium erinaceus, an edible and medicinal mushroom, displays various pharmacological activities in the prevention of dementia in conditions such as Parkinson’s and Alzheimer’s disease. The present study explored the neuroprotective effects of H. erinaceus mycelium polysaccharide-enriched aqueous extract (HE) on an l-glutamic acid (l-Glu)-induced differentiated PC12 (DPC12) cellular apoptosis model and an AlCl3 combined with d-galactose-induced Alzheimer’s disease mouse model.

https://www.mdpi.com/1422-0067/17/11/1810

Finding good food

Finding good food

I visited my local https://thesourcebulkfoods.com.au/ store at Rhodes the other day and found some great products. Among them was Kakadu plum powder and grass fed bone broth powder. The owner of the store and staff were very nice and very helpful. If you are looking for ingredients for your healthy meals then this is one good place to start. They have stores all around Australia and in some other regions as well and each seems to be owned by individuals or families under a franchise model. Each franchise also seems to have a fair bit of flexibility around sourcing ingredients so don’t be afraid to ask for something if it’s not already in store.

I will keep you up to date on new findings, please let us know if you find any places to get great quality ingredients.

Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

In recent years, natural products, which originate from plants, animals, and fungi, together with their bioactive compounds have been intensively explored and studied for their therapeutic potentials for various diseases such as cardiovascular, diabetes, hypertension, reproductive, cancer, and neurodegenerative diseases. Neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis are characterized by the progressive dysfunction and loss of neuronal structure and function that resulted in the neuronal cell death. Since the multifactorial pathological mechanisms are associated with neurodegeneration, targeting multiple mechanisms of actions and neuroprotection approach, which involves preventing cell death and restoring the function to damaged neurons, could be promising strategies for the prevention and therapeutic of neurodegenerative diseases. Natural products have emerged as potential neuroprotective agents for the treatment of neurodegenerative diseases. This review focused on the therapeutic potential of natural products and their bioactive compounds to exert a neuroprotective effect on the pathologies of neurodegenerative diseases.

https://www.hindawi.com/journals/ecam/2020/6565396/?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

The effects of resveratrol on lipid profiles and liver enzymes

The effects of resveratrol on lipid profiles and liver enzymes

This meta-analysis demonstrated that resveratrol supplementation among patients with MetS and related disorders significantly reduced total cholesterol and increased GGT concentrations, but did not affect triglycerides, LDL-, HDL-cholesterol, ALT, and AST concentrations. This data suggests that resveratrol may have a potential cardio-protective effect in patients with MetS and related disorders

https://link.springer.com/article/10.1186/s12944-020-1198-x?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Mitophagy and DNA damage signaling in human aging

Mitophagy and DNA damage signaling in human aging

Highlights

•DNA damage regulates mitophagy induction and mitochondrial homeostasis.

•Nuclear-mitochondrial signaling modulates aging and age-associated disorders.

•Combinatorial approaches targeting DNA repair and mitophagy could promote healthy aging.

Mitophagy and DNA damage signaling in human aging – ScienceDirect
Recent studies on anti-aging compounds with Saccharomyces cerevisiae as a model organism – ScienceDirect

Recent studies on anti-aging compounds with Saccharomyces cerevisiae as a model organism – ScienceDirect

Extension of lifespan and amelioration of aging-associated phenotypes have been targets of many studies. Some of the established methods of increasing lifespan including dietary restriction and genetic manipulation are difficult to apply to humans, and their side effects are hard to predict. For that reason, it is important to discover compounds that can mimic the anti-aging actions or induce lifespan extension through different metabolisms within the cell. Here we summarize the recent studies to test various types of compounds and materials using budding yeast that show potential anti-aging effects.

Recent studies on anti-aging compounds with Saccharomyces cerevisiae as a model organism – ScienceDirect
Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China – ScienceDirect

Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China – ScienceDirect

“By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0–58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0–13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα.”

https://www.sciencedirect.com/science/article/pii/S0140673620301835

Novel coronavirus 2019 (2019 n-CoV) – Fact sheets

Novel coronavirus 2019 (2019 n-CoV) – Fact sheets

What is a coronavirus?
Coronaviruses are a large family of viruses, some cause illness in humans, and others cause illness in animals, such as bats, camels, and civets. Human coronaviruses cause mild illness, such the common cold.

Rarely, animal coronaviruses can evolve to infect and spread among humans, causing severe diseases such as Severe Acute Respiratory Syndrome (SARS) which emerged in 2002, and Middle East Respiratory Syndrome (MERS) which emerged in 2012.

A novel coronavirus (2019-nCoV) is a new strain of coronavirus that has not been previously identified in humans.

What is 2019 novel coronavirus?
There is a new coronavirus affecting people who have recently been in the city of Wuhan, China. There is much more to learn about how it is spread, its severity, and other features associated with 2019-nCoV, and investigations are ongoing. At the moment, this coronavirus is called ‘novel coronavirus 2019’ or ‘2019-nCoV’.

Outbreaks of a novel coronavirus infections among people are always a public health concern. There is growing evidence that 2019-nCoV can spread from person to person in the community and in health care settings. There have been cases of 2019-nCoV reported in several Asian and other countries including Australia. The situation is evolving rapidly.

What are the symptoms?
Most case-patients have had fever, cough, and shortness of breath, with further evidence of pneumonia (chest infection).

Further investigation is required to assess whether there are undetected asymptomatic or mildly symptomatic cases.

How is it spread?
Early reports indicated that most of the cases had prior contact with a seafood and live animal market, suggesting an animal source of the outbreak. However, more recently, human to human transmission has been reported.

Further investigation is underway to confirm and describe the mode of transmission from animal sources, and the risk of human-to-human transmission.

Human to human transmission is most likely to be through direct contact with infectious patients, by respiratory droplets and by fomites (contaminated objects and surfaces), as is seen with other coronavirus infections including SARS and MERS.

Who is at risk?
People who are living or travelling to affected areas or who have had contact with other cases may be at risk of catching the disease. People with underlying illnesses that make them more vulnerable to respiratory disease, including those with diabetes, chronic lung disease, pre-existing kidney failure, people with suppressed immune systems and the elderly may be at a higher risk.

How is it prevented?
It’s likely that general prevention measures used for other coronavirus infections will also prevent infection with 2019-nCoV.

The World Health Organization (WHO) recommends measures to reduce the general risk of acute respiratory infections while travelling in or from affected areas by:

avoiding close contact with people suffering from acute respiratory infections;
frequent hand-washing, especially after direct contact with ill people or their environment;
avoiding close contact with live or dead farm or wild animals;
travellers with symptoms of acute respiratory infection should practice cough etiquette (maintain distance, cover coughs and sneezes with disposable tissues or clothing, and wash hands).
Travellers to China are already advised not to visit live bird and animal markets, including ‘wet’ markets, due to the risk of avian influenza.

There is currently no vaccine to prevent 2019-nCoV infections.

What should I do if I become unwell after travel in China?
If you become ill or feel unwell while travelling in China, you should not wait until you arrive back in Australia to seek medical assistance. Instead you should see a doctor or go to the local emergency department.

If you return from travel to China and feel unwell you should see your doctor or go to the emergency department to work out why you are ill, and you should mention your travel to China. Call ahead and explain that you might have been exposed to the novel coronavirus so that the doctor can make arrangements to see you quickly and safely.

How is it diagnosed?
Infection with 2019-nCoV is diagnosed by finding evidence of the virus in respiratory samples such as swabs from the throat or fluid from the lungs. Testing for 2019-nCoV is done in public health laboratories.

How is it treated?
There is currently no specific treatment for people who are sick with 2019-nCoV but general supportive medical care in hospital can be life-saving.

What is the public health response?
As of 23 January 2020, in Australia procedures to prevent the local spread of 2019-nCoV have been put in place.

Public health unit staff will investigate all cases to find out how the infection occurred, identify other people at risk of infection, implement control measures and provide other advice.

Further information
World Health Organization novel coronavirus information

NSW Health novel coronavirus alerts for GPs and hospital clinicians

For further information please call your local Public Health Unit on 1300 066 055

https://www.health.nsw.gov.au/Infectious/factsheets/Pages/novel-coronavirus.aspx

Kynurenine pathway, NAD+ synthesis, and mitochondrial function: Targeting tryptophan metabolism to promote longevity and healthspan – ScienceDirect

Kynurenine pathway, NAD+ synthesis, and mitochondrial function: Targeting tryptophan metabolism to promote longevity and healthspan – ScienceDirect

Highlights
• The kynurenine pathway has recently been identified as a promising target to increase healthy longevity.

• Targeted inhibition of kynurenine pathway activity may alleviate several pathological conditions and promote healthspan.

• Changes to the production and recycling of NAD+ is a likely mediator of the beneficial effects of kynurenine pathway interventions.

• Mitochondrial function and dynamics represent NAD+-dependent processes downstream of kynurenine metabolism that may mediate benefits during aging.

https://www.sciencedirect.com/science/article/pii/S053155651930765X

Aging and Caloric Restriction Modulate the DNA Methylation Profile of the Ribosomal RNA Locus in Human and Rat Liver

Aging and Caloric Restriction Modulate the DNA Methylation Profile of the Ribosomal RNA Locus in Human and Rat Liver

“We confirm previous findings, showing age-related hypermethylation, and describe, for the first time, that this gain in methylation also occurs in human hepatocytes. Furthermore, we show that age-related hypermethylation is enhanced in livers of rat upon CR at two and 10 months, and that at two months a trend towards the reduction of rRNA expression occurs. Collectively, our results suggest that CR modulates age-related regulation of methylation at the rDNA locus, thus providing an epigenetic readout of the pro-longevity effects of CR.”

https://www.mdpi.com/2072-6643/12/2/277

Understanding oxidants and antioxidants: Classical team with new players

Understanding oxidants and antioxidants: Classical team with new players

We talk about antioxidants a lot. Much of our longevity supplements are in fact antioxidants but, what are antioxidants and what is oxidisation and, furthermore, why do we care about it?

https://onlinelibrary.wiley.com/doi/abs/10.1111/jfbc.13145?af=R&utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound&sid=researcher

7-Day Easy Bulletproof Cyclical Ketosis Meal Plan (with Recipes)

7-Day Easy Bulletproof Cyclical Ketosis Meal Plan (with Recipes)

In the following link you’ll find a new post from Bulletproof, of Dave Asprey fame, about a proposed keto style diet plan complete with recipes.

7-Day Easy Bulletproof Cyclical Ketosis Meal Plan (with Recipes)
  • Health Hacker has no affiliation with Bulletproof and does not guarantee the content.
Resveralogues: From Novel Ageing Mechanisms to New Therapies? – Abstract – Gerontology – Karger Publishers

Resveralogues: From Novel Ageing Mechanisms to New Therapies? – Abstract – Gerontology – Karger Publishers

“For much of the 20th century the ageing process was thought to be the result of the interplay of many different biological processes, each with relatively small effects on organismal lifespan. However, this model is no longer tenable. Rather it seems a few biological mechanisms, including nutrient sensing, telomere attrition and cellular senescence, mediate large effects on health and longevity. Biogerontology may have suffered from initial delusions of complexity. However, we argue that it is premature to assume either that the list of biological processes influencing lifespan is now comprehensive or that these mechanisms act independently of each other.”

https://www.karger.com/Article/Abstract/504845

IJMS | Free Full-Text | BCL-xL, a Mitochondrial Protein Involved in Successful Aging: From C. elegans to Human Centenarians

IJMS | Free Full-Text | BCL-xL, a Mitochondrial Protein Involved in Successful Aging: From C. elegans to Human Centenarians

“B-Cell Lymphoma-extra-large (BCL-xL) is involved in longevity and successful aging, which indicates a role for BCL-xL in cell survival pathway regulation. Beyond its well described role as an inhibitor of apoptosis by preventing cytochrome c release, BCL-xL has also been related, indirectly, to autophagy and senescence pathways.”

https://www.mdpi.com/1422-0067/21/2/418?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis – ScienceDirect

NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis – ScienceDirect

Highlights
• NAD+ plays an important protective role in some age-related degenerative disease states.

• NAD+ can improve mitochondrial function and maintain sufficient levels of ATP.

• NAD+ can influences DNA repair, and immune and longevity processes.

• Raising NAD+ levels can balance energy needs with supply and protect against oxidative damage and inflammation.

• Further clinical trials are necessary to validate NAD+ therapy in ageing and disease.

https://www.sciencedirect.com/science/article/pii/S0531556519307582

The Healthy Grain BARLEYmax™ and Kebari Barley

The Healthy Grain BARLEYmax™ and Kebari Barley

Developed by CSIRO scientists, BARLEYmaxTM wholegrains represent the next evolution of superfoods, an enhanced wholegrain. The credentials of BARLEYmaxTM begin with it’s history. It was bred using traditional plant breeding processes, and is 100% GM free. The enhanced wholegrain discovered by Dr Morell and his team at the CSIRO contains two times the dietary fibre and four times the resistant starch of a regular grain.

The Healthy Grain BARLEYmax™ and Kebari Barley
Zinc transporters maintain longevity by influencing insulin/IGF‐1 activity in Caenorhabditis elegans – Novakovic – – FEBS Letters – Wiley Online Library

Zinc transporters maintain longevity by influencing insulin/IGF‐1 activity in Caenorhabditis elegans – Novakovic – – FEBS Letters – Wiley Online Library

“Adequate dietary intake of essential metals such as zinc is important for maintaining homeostasis. Abnormal zinc intake in Caenorhabditis elegans has been shown to increase or decrease normal lifespan by influencing the insulin/IGF‐1 pathway. Distribution of zinc is achieved by a family of highly conserved zinc transport proteins (ZIPT in C. elegans). This study investigated the role of the zipt family of genes and show that depletion of individual zipt genes results in a decreased lifespan”

https://febs.onlinelibrary.wiley.com/doi/abs/10.1002/1873-3468.13725

The somatic mutation landscape of the human body | Genome Biology | Full Text

The somatic mutation landscape of the human body | Genome Biology | Full Text

“Somatic mutations in healthy tissues contribute to aging, neurodegeneration, and cancer initiation, yet they remain largely uncharacterized.”

https://genomebiology.biomedcentral.com/articles/10.1186/s13059-019-1919-5

Study finds losing a night of sleep may increase blood levels of Alzheimer’s biomarker | EurekAlert! Science News

Study finds losing a night of sleep may increase blood levels of Alzheimer’s biomarker | EurekAlert! Science News

“A preliminary study by researchers at Uppsala University has found that when young, healthy men were deprived of just one night of sleep, they had higher levels of tau – a biomarker for Alzheimer’s disease – in their blood than when they had a full, uninterrupted night of rest. The study is published in the medical journal Neurology.”

https://www.eurekalert.org/pub_releases/2020-01/uu-sfl010820.php

Biologists identify pathways that extend lifespan by 500%

Biologists identify pathways that extend lifespan by 500%

“Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.

“Despite the discovery in C. elegans of cellular pathways that govern aging, it hasn’t been clear how these pathways interact,” said Hermann Haller, M.D., president of the MDI Biological Laboratory. “By helping to characterize these interactions, our scientists are paving the way for much-needed therapies to increase healthy lifespan for a rapidly aging population.””

https://phys.org/news/2020-01-biological-scientists-pathways-lifespan.html

What lifestyle changes will help me live longer and healthier?

We’ve previously spoken about how we might introduce foods and supplements to our diet to improve health span and lifespan. Here we explore activities and other therapies that show potential in living healthier and longer. We also explore things you perhaps should stop doing to improve health and longevity.

Mitochondrial support

Mitochondria are organelles, basically, little functional units within cells, much like an organ is to our body. They provide power to our cells by delivering ATP to the cells and are thought to once be free-ranging bacteria. It is thought that the break down of mitochondrial function is one of, if not the main contributor to aging.

Continue reading “What lifestyle changes will help me live longer and healthier?”

Which supplements can help me live longer and healthier?

There are two main ways to provide the nutrients and myriad of compounds that can help your body operate at its best and improve both lifespan and healthspan. One is to include foods and adjust your diet, however, we don’t always have that option to due various constraints such as taste and lifestyle. This is where supplements step in to provide the essential components of those foods as extracts or via chemical synthesis.

Here we explore the supplements you can incorporate into your lifestyle to get those identified goodies that keep us healthy for longer. This is the second of three articles on increasing health and life span. Our article on foods will have some overlap with this article as in many cases supplements are a derivative of food.
As always, we do our best to validate any information presented however, we cannot guarantee the accuracy of statements made here and does not constitute medical advice. Please check with your healthcare professional before making changes to your diet and lifestyle.
We have included as many references as possible to back our claims and for you to click into to investigate further for yourself. We encourage anyone seeking to improve their health via supplementation to take some time to research it’s effects, side effects and dosage.

Continue reading “Which supplements can help me live longer and healthier?”

Eating to live…longer and healthier.

There are two main ways to provide the nutrients and the myriad of compounds that can help your body operate at its best and improve both lifespan and healthspan. One is to use supplements and the other is to do it via food in our diet.

Here, in the first of our three part series on direct action for longevity, we explore the foods you can incorporate into your diet to get those identified goodies that keep us healthy for longer. We will also include herbs here as food as they require little to no handling to be beneficial and can be consumed as a food. Some of this is known via human clinical trial while some may be a mix of anecdotal use or animal studies. In all cases we take a can’t hurt, might help, approach and will either call out or exclude anything showing any risk of harm.

It’s important to note that, while all care is taken, we cannot guarantee the accuracy of this information and you should consult your health care professional before making changes in your diet and lifestyle.

Continue reading “Eating to live…longer and healthier.”
3 Ways We May Be Able To Reverse Aging, From A Microbiologist

3 Ways We May Be Able To Reverse Aging, From A Microbiologist

“Organic foods aren’t held with gloves. They’re a little bit more stressed out. The more stressed out your food is the brighter colors they’ll have because they’re producing these colors as a defense,” Sinclair explains.

Those bright colors, he adds, are indicators that the food has produced “xenohormesis molecules,” which activate our sirtuins that give our bodies an extra boost for longevity.

https://www.mindbodygreen.com/articles/3-easy-hacks-for-longevity-from-an-aging-microbiologist

Fisetin | | LEAF

Fisetin | | LEAF

“Fisetin, like many plant polyphenols, is known to have antioxidant properties and demonstrates the specific biological activity of protecting functional macromolecules against stress, resulting in a benefit to cellular cytoprotection. It is also known to have anti-inflammatory, chemopreventive, and chemotherapeutic properties.

Finally, more recently, it has also shown promise as a senolytic, a compound that encourages aged or damaged senescent cells to destroy themselves rather than lingering in the body and contributing to the chronic, age-related inflammation known as “inflammaging”, which is associated with a wide range of age-related diseases.

Since fisetin has a good safety profile, Mayo Clinic followed these mouse studies by launching three trials to see if the compound is effective for humans.”

Human Clinical Trials with Fisetin:

Fisetin | | LEAF

Australian Bushfire Relief: Where you can donate

Please excuse the slightly off topic post and thank you an advance for reading. We don’t like to stray from our core focus however, people’s lives and health are under threat.

As you may or may not be aware, Health Hacker is based in Sydney, Australia and our state, as well as neighbouring states have seen huge amounts of devastation over the last few months. Massive tracts of forests have been burned with countless animal losses and homes and human lives lost.

If you can help in any way but aren’t sure how, this is how:

TO HELP AFFECTED COMMUNITIES

Australian Red Cross Disaster Recovery and Relief
The Australian Red Cross is supporting communities affected by fires in NSW, QLD and SA. Volunteers are providing psychological first aid, working at evacuation centres and helping people to get in touch with their loved ones.
Where to donate: redcross.org.au/campaigns/disaster-relief-and-recovery-new-years-eve

Salvation Army Disaster Appeal
Salvation Army teams have been activated at multiple locations across the country. They are providing meals to evacuees and frontline responders, and will continue to provide whatever support is needed as the situation develops.
Where to donate: salvationarmy.org.au/donate/make-a-donation/donate-online/

St Vincent de Paul Society Bushfire Appeal
The St Vincent De Paul Society is running a NSW bushfire appeal, to help those affected with food, clothing, furniture, other essentials, and funds to pay bills.
Where to donate: donate.vinnies.org.au/appeals-nsw/vinnies-nsw-bushfire-appeal-nsw

Givit
Givit is encouraging people to donate funds or specific items requested by residents.
Where to donate: givit.worldsecuresystems.com/items-needed

Foodbank
Foodbank is delivering emergency food relief and water to firefighters and local communities caught up in the bushfires.
Where to donate: foodbank.org.au/support-us/make-a-donation/

TO HELP FIREFIGHTERS

Support firefighter families
Donate to the families of the volunteer firefighters who were tragically killed while on duty.
Where to donate: rfs.nsw.gov.au/news-and-media/general-news/featured/support-for-firefighter-families

TO HELP WILDLIFE

WIRES
WIRES is accepting donations to help their efforts in supporting displaced and injured wildlife.
Where to donate: wires.org.au/donate/emergency-fund

Koalas in Care Inc
Koalas in Care Inc are accepting donations to help koalas injured or displaced by the fires in NSW.
Where: to donate: koalasincare.org.au/pages/donation.htm

The Port Macquarie Koala Hospital
The Port Macquarie Koala Hospital is accepting donations to develop and build watering stations for thirsty koalas.
Where to donate: gofundme.com/f/help-thirsty-koalas-devastated-by-recent-fires

Taken from:

http://www.mygc.com.au/bushfire-relief-where-you-can-donate/

Thank you for your time.

Centenarians: An excellent example of resilience for successful ageing – ScienceDirect

Centenarians: An excellent example of resilience for successful ageing – ScienceDirect

Highlights
• Centenarians maintain intrinsic capacity longer than individuals who display ordinary aging.

• Resilience is a determinant of health, and centenarians maintain it longer.

• Centenarians have specific genetic features.

https://www.sciencedirect.com/science/article/abs/pii/S0047637419302040

Role of High‐Density Lipoproteins in Cholesterol Homeostasis and Glycemic Control | Journal of the American Heart Association

Role of High‐Density Lipoproteins in Cholesterol Homeostasis and Glycemic Control | Journal of the American Heart Association

Emerging evidence (summarized in Table) indicates that HDL‐ and apoA‐I–targeted therapies are a potential option for conserving residual β‐cell function and improving insulin sensitivity in patients who are progressing toward, or have already developed, T1DM and T2DM. The recent failures of HDL‐raising agents in cardiovascular clinical outcome trials highlight the need to develop novel and innovative HDL‐targeted approaches to achieve these goals. Elucidating the mechanism(s) underlying the antidiabetic functions of HDLs and apoA‐I will also provide opportunities to identify and develop new HDL‐targeted therapies for diabetes mellitus. Achievement of these goals could be particularly advantageous for patients with T1DM for whom treatment options are currently limited to insulin replacement therapy, and for patients with T2DM that are refractory to currently available therapies.

Table 1.Role of HDL and apoA‐I in Glycemic Control, Insulin Sensitivity and β‐Cell Function
Topic Outcome Reference
Association of HDL‐C and apoA‐I levels with glycemic control
Subjects with T2DM Serum HDL‐C, apoA‐I, and HDL‐C/apoA‐I levels are inversely associated with insulin resistance by HOMA‐IR 9
Subjects with impaired glucose tolerance ApoA‐I level is an independent risk factor for glucose tolerance 10
HDL and apoA‐I in glucose disposal/insulin sensitivity
Primary human skeletal muscle cells ApoA‐I improves insulin‐dependent and ‐independent glucose uptake 27
C2C12 skeletal muscle cells ApoA‐I increases glucose uptake by phosphorylation of AMPK 35
High‐fat–fed C57BL/6 mice ApoA‐I improves insulin sensitivity by reducing systemic and hepatic inflammation 40
db/db mice Long‐term HDL infusion improves glucose tolerance by activating GSK‐3 and AMPK in skeletal muscle 37
Pregnant female Wistar rats ApoA‐I infusions increase insulin sensitivity, reduces systemic inflammation and protects against pregnancy‐induced insulin resistance 45
Subjects with T2DM A single rHDL infusion reduces plasma glucose levels by increasing insulin secretion and promoting glucose uptake in skeletal muscle 2
HDL and apoA‐I in β‐cell function
Min6 insulinoma cells HDLs isolated from normal human plasma, rHDLs, and apoA‐I increase Ins1 and Ins2 gene transcription and GSIS 58
Ins‐1E insulinoma cells ApoA‐I increases Pdx1 gene transcription and GSIS 57
βTC3 insulinoma cells Incubation with HDL protects βTC3 cells against LDL‐induced apoptosis 70
C57BL/6 mice ApoA‐I infusions increase insulin secretion and improve glucose tolerance 52
High‐fat–fed C57BL/6 mice Short‐term apoA‐I treatment increases GSIS and improves glucose clearance independent of insulin secretion 53
Mice with conditional deletion of ABCA1 and ABCG1 in β cells ApoA‐I infusions increase GSIS in islets isolated from mice with elevated islet cholesterol levels 54
Healthy subjects and Min6 cells CETP inhibition increases plasma HDL‐C, apoA‐I, and insulin levels in normal human subjects. Plasma from these subjects also increases GSIS in Min6 cells pretreated with oxidized LDLs 60
Isolated human islets HDL protects human islets against oxidized LDL‐induced apoptosis 71
Isolated human and mouse islets HDL protects human and mouse islets from interleukin‐1β– and glucose‐induced apoptosis 72
AMPK indicates adenosine monophosphate‐activated protein kinase; apoA‐I, apolipoprotein A‐I; CETP, cholesteryl ester transfer protein; GSIS, glucose‐stimulated insulin secretion; GSK, glycogen synthase kinase‐3; HDL, high‐density lipoprotein; HDL‐C, high‐density lipoprotein cholesterol; HOMA‐IR, Homeostatic model assessment of insulin resistance; LDL, low‐density lipoprotein; rHDL, reconstituted HDL.

https://www.ahajournals.org/doi/10.1161/JAHA.119.013531

The Vagus Nerve is Key to Well-Being | Elemental

The Vagus Nerve is Key to Well-Being | Elemental

“The vagus nerve, also called the “10th cranial nerve,” is the longest, largest, and most complex of the cranial nerves, and in some ways it’s also the least understood. Experts have linked its activity to symptom changes in people with migraine headaches, inflammatory bowel disease, depression, epilepsy, arthritis, and many other common ailments. The more science learns about the vagus nerve, the more it seems like a better understanding of its function could unlock new doors to treating all manner of human suffering.”

https://elemental.medium.com/science-confirms-that-the-vagus-nerve-is-key-to-well-being-c23fab90e211

Muscle wasting disease linked to defective mitochondrial energy and NAD+ biosynthesis pathways – Science Mission

Muscle wasting disease linked to defective mitochondrial energy and NAD+ biosynthesis pathways – Science Mission

“Moreover, results showed that sarcopenia was also associated with reduced levels of enzymes involved in the recycling of NAD+, which acts as a metabolic sensor in the cell and regulates energy production pathways.”

http://sciencemission.com/site/index.php?page=news&type=view&id=health-science%2Fmuscle-wasting-disease&filter=8%2C9%2C10%2C11%2C12%2C13%2C14%2C16%2C17%2C18%2C19%2C20%2C27

Mitochondrial Haplogroups and Lifespan in a Population Isolate – ScienceDirect

Mitochondrial Haplogroups and Lifespan in a Population Isolate – ScienceDirect

“The lifespan-lengthening association was apparent in both sexes but only after the age of 60. Our results provide further support for the role of mitochondrial genetics in lengthening human lifespan.”

https://www.sciencedirect.com/science/article/abs/pii/S1567724919301047

Why 80 Percent of New Year’s Resolutions Fail

A new year, and a new decade lay before us as we reach the end of 2019.

You’re inspired to start improving something about your health of life.

Don’t, well, more accurately do, but don’t do it for a new years resolution.

Do it because you are ready, do it because you’re done with the status quo, do it for your happiness, for your family.

Do it for any reason other than an arbitrary date with artificial importance projected upon it.

Changes are hard and habits are strong. It takes time and conviction to change so you need to be truly ready and you need to do it as soon as you can.

If you set yourself a new years resolution and fail you are likely to give up completely or revert back to comfort to relive the disappointment and depression that may follow a failed new years resolution.

Know that you have it in you to change without an arbitrary date. You can do it!

from:

https://health.usnews.com/health-news/blogs/eat-run/articles/2015-12-29/why-80-percent-of-new-years-resolutions-fail

Effects of Intermittent Fasting on Health, Aging, and Disease | NEJM

Effects of Intermittent Fasting on Health, Aging, and Disease | NEJM

“Evidence is accumulating that eating in a 6-hour period and fasting for 18 hours can trigger a metabolic switch from glucose-based to ketone-based energy, with increased stress resistance, increased longevity, and a decreased incidence of diseases, including cancer and obesity.”

https://www.nejm.org/doi/full/10.1056/NEJMra1905136

Longevity protein SIRT6 also protects against fatty liver and fatty liver disease – Science Mission

Longevity protein SIRT6 also protects against fatty liver and fatty liver disease – Science Mission

“Fatty liver, or hepatic steatosis, which develops when the body produces too much fat or doesn’t metabolize fat efficiently enough, affects around 25% of the global population. Excess fat is stored in liver cells, where it accumulates and can cause fatty liver and other diseases.

In a study just published in the journal Cell Reports, researchers reveal for the first time that SIRT6, a protein involved in regulating many biological processes such as aging, obesity, insulin resistance, inflammation and metabolism, also plays a crucial role in burning and regulating liver fat metabolism.”

http://sciencemission.com/site/index.php?page=news&type=view&id=health-science%2Flongevity-protein-sirt6&filter=8%2C9%2C10%2C11%2C12%2C13%2C14%2C16%2C17%2C18%2C19%2C20%2C27

Age and life expectancy clocks based on machine learning analysis of mouse frailty | bioRxiv

Age and life expectancy clocks based on machine learning analysis of mouse frailty | bioRxiv

“The identification of genes and interventions that slow or reverse aging is hampered by the lack of non-invasive metrics that can predict life expectancy of pre-clinical models. Frailty Indices (FIs) in mice are composite measures of health that are cost-effective and non-invasive, but whether they can accurately predict health and lifespan is not known. Here, mouse FIs were scored longitudinally until death and machine learning was employed to develop two clocks. ”

https://www.biorxiv.org/content/10.1101/2019.12.20.884452v1

Evidence-Based Eating Guide | NutritionFacts.org

Evidence-Based Eating Guide | NutritionFacts.org

The Evidence-Based Eating Guide: A Healthy Living Resource from Dr. Greger & NutritionFacts.org is a tool designed to help make the switch to a healthier lifestyle more simple. It’s an easy to understand guide with applicable information for eating healthier, including a breakdown of Dr. Greger’s Traffic Light Eating, tips for using Dr. Greger’s Daily Dozen checklist, sample menus, and more.

https://nutritionfacts.org/healthkit/

The State of Ageing in 2019: Adding life to our years | Centre for Ageing Better

The State of Ageing in 2019: Adding life to our years | Centre for Ageing Better

How prepared is society for our longer lives? Our new report, ‘The State of Ageing in 2019’, uses publicly available data to give a snapshot of what life is like for people aged 65 and older today. It also investigates the prospects for people currently in their 50s and 60s looking across four crucial areas: work and finances, housing, health and communities.

The State of Ageing in 2019: Adding life to our years

https://www.ageing-better.org.uk/publications/state-of-ageing-2019

Weight for it: Time-restricted eating benefits those at risk for diabetes, heart disease | EurekAlert! Science News

Weight for it: Time-restricted eating benefits those at risk for diabetes, heart disease | EurekAlert! Science News

“The pilot study, published online in the December 5, 2019 edition of Cell Metabolism, found that when participants restricted their eating to 10 hours or less over a period of 12 weeks, they lost weight, reduced abdominal fat, lowered blood pressure and cholesterol and enjoyed more stable blood sugar and insulin levels.”

https://www.eurekalert.org/pub_releases/2019-12/uoc–wfi120519.php

Anti-inflammatory, analgesic and acute toxicity effects of fermented soybean | BMC Complementary and Alternative Medicine | Full Text

Anti-inflammatory, analgesic and acute toxicity effects of fermented soybean | BMC Complementary and Alternative Medicine | Full Text

NESTE is a nutritious food ingredient with potential anti-inflammatory and analgesic effects.

https://bmccomplementalternmed.biomedcentral.com/articles/10.1186/s12906-019-2791-2

Medium Chain Triglycerides induce mild ketosis and may improve cognition in Alzheimer’s disease. A systematic review and meta-analysis of human studies – ScienceDirect

Medium Chain Triglycerides induce mild ketosis and may improve cognition in Alzheimer’s disease. A systematic review and meta-analysis of human studies – ScienceDirect

Highlights

From meta-analysis of RCTs in Alzheimer’s disease and Mild Cognitive Impairment, oral Medium Chain Triglycerides administration induced mild peripheral ketosis


From meta-analysis of RCTs in Alzheimer’s disease and Mild Cognitive Impairment, oral Medium Chain Triglycerides administration improved cognition on a combined scale of ADAS-Cog and MMSE.


Risk of bias of existing studies of RCTs in Alzheimer’s disease and Mild Cognitive Impairment necessitates future trials.

https://www.sciencedirect.com/science/article/pii/S156816371930131X

A small molecule transcription factor EB activator ameliorates beta‐amyloid precursor protein and Tau pathology in Alzheimer’s disease models – Song – – Aging Cell – Wiley Online Library

A small molecule transcription factor EB activator ameliorates beta‐amyloid precursor protein and Tau pathology in Alzheimer’s disease models – Song – – Aging Cell – Wiley Online Library

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13069?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

Frontiers | Intense Physical Exercise Induces an Anti-inflammatory Change in IgG N-Glycosylation Profile | Physiology

Frontiers | Intense Physical Exercise Induces an Anti-inflammatory Change in IgG N-Glycosylation Profile | Physiology


” Exercise is known to improve many aspects of human health, including modulation of the immune system and inflammatory status. It is generally understood that exercise reduces inflammation, but there are missing links in terms of understanding the mechanisms as well as the differences between exercise modalities. N-glycosylation of immunoglobulin G (IgG) and total plasma proteins was previously shown to reflect changes in inflammatory pathways, which could provide valuable information to further clarify exercise effects. In order to further expand the understanding of the relationship between physical activity and inflammation, we examined the effect of intense exercise, in the form of repeated sprint training (RST), on IgG and total plasma proteins N-glycosylation in combination with traditionally used inflammation markers: C-reactive protein (CRP), interleukin 6 (IL-6), and leukocyte count.

https://www.frontiersin.org/articles/10.3389/fphys.2019.01522/full?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Potassium channels in the neuronal homeostasis and neurodegenerative pathways underlying Alzheimer’s Disease: an update – ScienceDirect

Potassium channels in the neuronal homeostasis and neurodegenerative pathways underlying Alzheimer’s Disease: an update – ScienceDirect

Highlights

•Potassium (K+) channels are key regulators of cell excitability in several tissues.

•A dysregulation of K+ channels is associated with Alzheimer’s disease (AD).

•The role of K+ channels in AD is not completely elucidated.

•Understanding their functions will be helpful for clarifying AD pathogenesis.

•Modulating K+ channel expression should be useful for developing novel drugs.

Potassium channels in the neuronal homeostasis and neurodegenerative pathways underlying Alzheimer’s Disease: an update – ScienceDirect
Chinese Herbal Medicine Formula Shenling Baizhu San Ameliorates High-Fat Diet-Induced NAFLD in Rats by Modulating Hepatic MicroRNA Expression Profiles

Chinese Herbal Medicine Formula Shenling Baizhu San Ameliorates High-Fat Diet-Induced NAFLD in Rats by Modulating Hepatic MicroRNA Expression Profiles

“Objective. The purpose of present study was to investigate the potential mechanism underlying the protective effect of Shenling Baizhu San (SLBZS) on nonalcoholic fatty liver disease (NAFLD) by microRNA (miRNA) sequencing. Methods. Thirty male Wistar rats were randomly divided into a normal control (NC) group, a high-fat diet (HFD) group, and an SLBZS group. After 12 weeks, the biochemical parameters and liver histologies of the rats were assessed. The Illumina HiSeq 2500 sequencing platform was used to analyse the hepatic miRNA expression profiles. Representative differentially expressed miRNAs were further validated by qRT-PCR. The functions of the differentially expressed miRNAs were analysed by bioinformatics. Results. Our results identified 102 miRNAs that were differentially expressed in the HFD group compared with the NC group. Among those differentially expressed miRNAs, the expression levels of 28 miRNAs were reversed by SLBZS administration, suggesting the modulation effect of SLBZS on hepatic miRNA expression profiles. The qRT-PCR results confirmed that the expression levels of miR-155-5p, miR-146b-5p, miR-132-3p, and miR-34a-5p were consistent with those detected by sequencing. Bioinformatics analyses indicated that the target genes of the differentially expressed miRNAs reversed by SLBZS were mainly related to metabolic pathways. Conclusion. This study provides novel insights into the mechanism of SLBZS in protecting against NAFLD; this mechanism may be partly related to the modulation of hepatic miRNA expression and their target pathways.”

Chinese Herbal Medicine Formula Shenling Baizhu San Ameliorates High-Fat Diet-Induced NAFLD in Rats by Modulating Hepatic MicroRNA Expression Profiles
DNA Testing

DNA Testing

Have you considered getting your DNA sequenced? Wonder what kind of information you could expect out of it?

I recently got my DNA sequenced at Self Decode and the results are in! Let’s take a look at whats in there and how I might be able to use it to improve my health and lifespan.

The introductory report shows me a high level overview of things I may want to dig deeper into.

Now, what does this mean and what can I do about it?

Typical risk of vit. k deficiency so, not much needed to be done here
Mostly typical ability to convert beta-carotene to Vit. A. Nothing to see here.
Seemingly normal ability to process B12. Good news.
I know I have one of two MTFHR gene mutations so no surprises here on Folate. I supplement with MTHF or Methyl-Folate to make up for this.
Now, I don’t drink Coffee, nor do I drink and caffeinated drinks so, nothing to worry about here. Basically I can process caffeine more readily.
Need to keep an eye on food intake. I have recently started intermittent fasting and have reduce my sugar and dairy intake (see our post about miRNA’s in milk expressing mTOR and suppressing AMPK).
Mix results here meaning no real action needed except that I should possibly target power training.
Typical Lipid levels. Not better or worse, just your regular ability to process lipids.
I never considered that DNA may influence something like my levels of empathy. I guess this explains why I’ve started Health Hacker to help people live healthier and longer lives.
Look out Black Friday and Cyber Monday, here comes an impulse shopper!
Anxiety is something I’ve struggled with for most of my life. I employ multiple strategies to help with it including CBD and B3, along with Omega-3.

Along with the report are sources to NIH publications to back the assertions. You also get deeper reports on each of those subject areas including MTFHR, APOE, Mood, Cognitive, Essential Minerals, Vitamins, Sleep, Cardiovascular, Inflammation and Fitness. You also get a personalised blog that shows you articles related to SNPs in your results.

I’m not saying that this is the best DNA service but it’s the one I chose and this is what I got. It seems quite comprehensive and does a good job at explaining what it all means and how I can adjust my diet and lifestyle to account for deficiencies caused by gene mutations. If this is something you are interested in then it might be an option for you.

LB100 ameliorates nonalcoholic fatty liver disease via the AMPK/Sirt1 pathway

LB100 ameliorates nonalcoholic fatty liver disease via the AMPK/Sirt1 pathway

“PP2A inhibition by LB100 significantly ameliorates hepatic steatosis by regulating hepatic lipogenesis and fatty acid oxidation via the AMPK/Sirt1 pathway. LB100 may be a potential therapeutic agent for NAFLD.”

https://www.wjgnet.com/1007-9327/full/v25/i45/6607.htm

Mechanisms of Calorie Restriction: A Review of Genes Required for the Life-Extending and Tumor-Inhibiting Effects of Calorie Restriction

Mechanisms of Calorie Restriction: A Review of Genes Required for the Life-Extending and Tumor-Inhibiting Effects of Calorie Restriction

” We reviewed and discussed underlying mechanisms of CR from an aspect of CR genes. It should be stressed that the isoform specificity of FoxO transcription factors for longevity becomes apparent under CR conditions but not AL conditions. Npy and FoxO1 both play pleiotropic roles in aging and related disorders, depending on the nutritional state. As briefly described in Section 1 and Section 2, the life-extending effects of CR and reduced IGF-1 signaling are also sexually dimorphic. Genes associated with regulation of the aging process should be investigated carefully in a context-dependent manner, i.e., abilities of physiological adaptation for individuals against environmental challenges, particularly food shortage. “

https://www.mdpi.com/2072-6643/11/12/3068/htm

Protein intake and transitions between frailty states and to death in very old adults: the Newcastle 85+ study

Protein intake and transitions between frailty states and to death in very old adults: the Newcastle 85+ study

“High protein intake, partly mediated by energy intake, may delay incident frailty in very old adults. Frailty prevention strategies in this age group should consider adequate provision of protein and energy.”

Emerging Role of C/EBPβ and Epigenetic DNA Methylation in Ageing: Trends in Genetics

Emerging Role of C/EBPβ and Epigenetic DNA Methylation in Ageing: Trends in Genetics

“Ageing is closely associated with and influenced by energy metabolism, and C/EBPβ is emerging as a key regulator of energy metabolism and longevity.”

https://www.cell.com/trends/genetics/fulltext/S0168-9525(19)30245-8?dgcid=raven_jbs_aip_email

12 Ways To Upgrade Your Lifespan & Healthspan IQ

12 Ways To Upgrade Your Lifespan & Healthspan IQ

The amount of time we live is called lifespan. The length of time that a person is healthy and functional—not just alive—is called healthspan. Scientific understanding in these areas is advancing rapidly. Below are 12 things the collective thinks will help on your journey to a longer healthier you. 

1. BOOST NAD+ LEVELS

2. POWER UP WITH ATP

3. CREATE FIT MITOCHONDRIA

4. ACTIVATE AMPK

5. CALORIE RESTRICTION AND CALORIE RESTRICTION MIMETICS

6. EXERCISE AND EXERCISE MIMETICS

7. BODY CLOCK 

8. FOLLOW A HEALTHY AGING EXPERT

12 Ways To Upgrade Your Lifespan & Healthspan IQ

Mitochondria: Exploring 5 Lifestyle Habits to Benefit Cell Health

Mitochondria: Exploring 5 Lifestyle Habits to Benefit Cell Health

In each of our cells are small energy generators called mitochondria. The health of our mitochondria determines the amount of adenosine triphosphate (ATP) they can produce from the calories we eat and oxygen we consume. Without robust mitochondria, cells cannot do as much work as they’re capable of and we need them to do so we can stay healthy. To achieve higher levels of performance we must optimize our mitochondria, the powerhouse of our cells, to produce energy. Cell function isn’t always the first place biohackers and nootropics enthusiasts start because it is challenging to notice a subjective boost in our mitochondrial function. Whether we can detect enhanced mitochondria subjectively or not, the science is pretty clear that healthy mitochondria play a role in supporting all indicators of cognition, physical performance, and aging. In a series of comprehensive posts, we will introduce scientifically-backed lifestyle changes and nootropics that up-regulate your mitochondrial function. In our last post, we went over how to use light and temperature to boost mitochondria. Now let’s tackle 5 more lifestyle habits we can implement to achieve healthier mitochondria.

Mitochondria: Exploring 5 Lifestyle Habits to Benefit Cell Health

Maf1‐dependent transcriptional regulation of tRNAs prevents genomic instability and is associated with extended lifespan – Shetty – – Aging Cell – Wiley Online Library

Maf1‐dependent transcriptional regulation of tRNAs prevents genomic instability and is associated with extended lifespan – Shetty – – Aging Cell – Wiley Online Library

Fundamental cellular mechanisms such as nutrient sensing, DNA damage response pathways, and cell cycle regulation influence the aging process. Studies have shown that the nutrient sensory kinase, mTOR (TOR in yeast), regulates lifespan in response to nutrient availability. The mTOR kinase forms two distinct protein complexes: TORC1 and TORC2. TORC1, which is inhibited by rapamycin, regulates cell growth, proliferation, and metabolism. It is well established that TORC1 promotes protein translation via phosphorylation of ribosomal protein S6 kinase and the eIF4E‐binding protein (BP; Zoncu, Efeyan, & Sabatini, 2011). The TORC2 branch is less studied; however, TORC2 also plays important roles in metabolism, cell survival, and proliferation (Zoncu et al., 2011). Although the involvement of the TORC1 pathway in lifespan regulation is conserved among many species (i.e., TORC1 inhibition extends lifespan), it is still unclear how this pathway affects multiple downstream stress and damage response mechanisms.

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13068?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

Measuring biological aging in humans: A quest – Ferrucci – – Aging Cell – Wiley Online Library

Measuring biological aging in humans: A quest – Ferrucci – – Aging Cell – Wiley Online Library

“The global population of individuals over the age of 65 is growing at an unprecedented rate and is expected to reach 1.6 billion by 2050. Most older individuals are affected by multiple chronic diseases, leading to complex drug treatments and increased risk of physical and cognitive disability. Improving or preserving the health and quality of life of these individuals is challenging due to a lack of well‐established clinical guidelines. Physicians are often forced to engage in cycles of “trial and error” that are centered on palliative treatment of symptoms rather than the root cause, often resulting in dubious outcomes. Recently, geroscience challenged this view, proposing that the underlying biological mechanisms of aging are central to the global increase in susceptibility to disease and disability that occurs with aging. In fact, strong correlations have recently been revealed between health dimensions and phenotypes that are typical of aging, especially with autophagy, mitochondrial function, cellular senescence, and DNA methylation. Current research focuses on measuring the pace of aging to identify individuals who are “aging faster” to test and develop interventions that could prevent or delay the progression of multimorbidity and disability with aging. Understanding how the underlying biological mechanisms of aging connect to and impact longitudinal changes in health trajectories offers a unique opportunity to identify resilience mechanisms, their dynamic changes, and their impact on stress responses. Harnessing how to evoke and control resilience mechanisms in individuals with successful aging could lead to writing a new chapter in human medicine.”

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13080?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

The strange case of AMPK and cancer: Dr Jekyll or Mr Hyde?† | Open Biology

The strange case of AMPK and cancer: Dr Jekyll or Mr Hyde?† | Open Biology

“The AMP-activated protein kinase (AMPK) acts as a cellular energy sensor. Once switched on by increases in cellular AMP : ATP ratios, it acts to restore energy homeostasis by switching on catabolic pathways while switching off cell growth and proliferation. The canonical AMP-dependent mechanism of activation requires the upstream kinase LKB1, which was identified genetically to be a tumour suppressor. AMPK can also be switched on by increases in intracellular Ca2+, by glucose starvation and by DNA damage via non-canonical, AMP-independent pathways. Genetic studies of the role of AMPK in mouse cancer suggest that, before disease arises, AMPK acts as a tumour suppressor that protects against cancer, with this protection being further enhanced by AMPK activators such as the biguanide phenformin. However, once cancer has occurred, AMPK switches to being a tumour promoter instead, enhancing cancer cell survival by protecting against metabolic, oxidative and genotoxic stresses. Studies of genetic changes in human cancer also suggest diverging roles for genes encoding subunit isoforms, with some being frequently amplified, while others are mutated.”

https://royalsocietypublishing.org/doi/10.1098/rsob.190099?utm_source=researcher-app&utm_medium=researcherad&utm_campaign=DVaughan_Promotedpaper_190099&utm_content=Paper

Frontiers | Physiological and Epigenetic Features of Yoyo Dieting and Weight Control

Frontiers | Physiological and Epigenetic Features of Yoyo Dieting and Weight Control

“Obesity and being overweight have become a worldwide epidemic affecting more than 1.9 billion adults and 340 million children. Efforts to curb this global health burden by developing effective long-term non-surgical weight loss interventions continue to fail due to weight regain after weight loss. Weight cycling, often referred to as Yoyo dieting, is driven by physiological counter-regulatory mechanisms that aim at preserving energy, i.e. decreased energy expenditure, increased energy intake, and impaired brain-periphery communication. Models based on genetically determined set points explained some of the weight control mechanisms, but exact molecular underpinnings remained elusive. Today, gene–environment interactions begin to emerge as likely drivers for the obesogenic memory effect associated with weight cycling. Here, epigenetic mechanisms, including histone modifications and DNA methylation, appear as likely factors that underpin long-lasting deleterious adaptations or an imprinted obesogenic memory to prevent weight loss maintenance.”

Dietary inflammatory index and mortality

Dietary inflammatory index and mortality

“Higher Dietary Inflammatory Index (DII®) scores are associated with increased morbidity and mortality. However, little is known about the effects of DII on mortality in Mediterranean countries. Therefore, in the present study, we aimed to investigate the potential association between DII scores and overall, cancer and cardiovascular disease (CVD) mortality in people living in a Mediterranean area.”

“Higher DII scores were associated with a significantly higher mortality risk, whereas the association with cause‐specific mortality was less clear. These findings highlight the potential importance of diet in modulating inflammation and preventing death. ”

Dietary inflammatory index and mortality: a cohort longitudinal study in a Mediterranean area – Veronese – – Journal of Human Nutrition and Dietetics – Wiley Online Library

Exercise Intervention Helps Slow Down Memory Loss – Conduct Science

Exercise Intervention Helps Slow Down Memory Loss – Conduct Science

“Mild cognitive impairment or cognitive impairment without dementia (CIND) is a health condition elderly people suffer from.
The condition causes memory loss and in extreme cases, it can progress to Alzheimer’s disease.
A new study shows that exercise may help elevate symptoms of the condition.”

https://conductscience.com/exercise-intervention-helps-slow-down-memory-loss/

Sync all of your health data and trackers with “Health Sync”

Sync all of your health data and trackers with “Health Sync”

No referral or benefit, I just found this super useful and it allows me to bring my fitbit weight and oura sleep into Samsung health and Google fit.

It also supports Suunto, Garmin and many others.

https://play.google.com/store/apps/details?id=nl.appyhapps.healthsync

Researchers discover brain circuit linked to food impulsivity: This creates the possibility scientists can someday develop therapeutics to address overeating — ScienceDaily

Researchers discover brain circuit linked to food impulsivity: This creates the possibility scientists can someday develop therapeutics to address overeating — ScienceDaily

https://www.sciencedaily.com/releases/2019/12/191211145630.htm

Alzheimer’s drug candidates reverse broader aging, study shows — ScienceDaily

Alzheimer’s drug candidates reverse broader aging, study shows — ScienceDaily

” In mouse models of Alzheimer’s disease, the investigational drug candidates known as CMS121 and J147 improve memory and slow the degeneration of brain cells. Now, researchers have shown how these compounds can also slow aging in healthy older mice, blocking the damage to brain cells that normally occurs during aging and restoring the levels of specific molecules to those seen in younger brains.”

https://www.sciencedaily.com/releases/2019/12/191210134028.htm

Skin Rejuvenation by Low-Level Light Therapy

Skin Rejuvenation by Low-Level Light Therapy

Risk-Benefit Analysis

Forever Healthy Foundation gGmbH

Amalienbadstraße 41

D-76227 Karlsruhe, Germany

Low-level light therapy (LLLT) is the use of low incident levels of photon energy at a particular wavelength, targeting tissue to achieve a clinically useful local or systemic effect without the creation of heat (athermal) or damage (atraumatic) (Calderhead & Tanaka, 2017). LLLT has shown dramatic effects when used for wound healing, pain management, and various musculoskeletal conditions.

This review focuses on its potential use in skin rejuvenation. It has been shown that upon exposure to light, chromophores in the skin (mitochondrial cytochrome C, melanin, and protoporphyrins) absorb photons which lead to downstream alterations in physiology such as changes in cell proliferation, differentiation, migration, inflammatory mediators, and collagen production. It is supposed that these photobiomodulative effects have beneficial effects on the skin, leading to a more youthful appearance through increased collagen and elastin production, and a reduction in age spots and wrinkles. 

Key Questions 

This analysis seeks to answer the following questions:

  • Which benefits with regard to skin rejuvenation result from LLLT? 
  • Which risks are involved in using LLLT for skin rejuvenation (general and method-specific)?
  • What are the potential risk mitigation strategies?
  • Which method/device or combination of methods/devices is most effective for skin rejuvenation using LLLT?
  • Which of the available devices/methods are safe for use? 
  • What is the best therapeutic protocol available at the moment?  

https://brain.forever-healthy.org/display/EN/Skin+Rejuvenation+by+Low-Level+Light+Therapy

Fisetin Senolytic Therapy

Fisetin Senolytic Therapy

Risk-Benefit Analysis

Forever Healthy Foundation gGmbH

Amalienbadstraße 41

D-76227 Karlsruhe, Germany

Senolytics are agents that selectively induce apoptosis of senescent cells. Fisetin is a flavonoid polyphenol found in many types of fruits and vegetables (Arai et al., 2000) that is believed to act as a senolytic in addition to its numerous other known benefits. Although natural senolytics are less potent, compared to the targeted senolytics, they have lower toxicity and are thus, likely to be more readily translatable to clinical medicine. This RBA focuses on the risks and benefits of using fisetin as a senolytic rather than its more common use as a supplement.

Key Questions 

This RBA seeks to answer the following questions:

  • Which health and/or longevity benefits result from the use of fisetin as a senolytic? 
  • Which risks are involved in the use of fisetin as a senolytic (general and method-specific)?
  • What are the potential risk mitigation strategies?
  • Which method or combination of methods of using fisetin as a senolytic are most effective?
  • Which of the available methods are safe for use?
  • What is the best therapeutic protocol available at the moment?  

https://brain.forever-healthy.org/display/EN/Fisetin+Senolytic+Therapy

NAD+ Restoration Therapy

NAD+ Restoration Therapy

Risk-Benefit Analysis

Forever Healthy Foundation gGmbH

Amalienbadstraße 41

D-76227 Karlsruhe, Germany

NAD+ is a pyridine nucleotide found in all living cells. It plays an important role in energy metabolism and is a substrate for several enzymes (including those involved in DNA repair). NAD+ levels may decline markedly with age (Massudi et al., 2012Clement et al., 2019Zhu et al., 2011) and restoring those levels to a youthful state is believed to have beneficial effects on health and longevity. 

Key Questions 

This analysis seeks to answer the following questions:

  • Which health and/or longevity benefits result from raising NAD+ levels in humans? 
  • Which risks are involved in raising NAD+ levels (general and method-specific)?
  • What are the potential risk mitigation strategies?
  • Which method or combination of methods is most effective in raising NAD+ levels?
  • Which of the available methods are safe for use? 
  • What is the best therapeutic protocol available at the moment?  

https://brain.forever-healthy.org/display/EN/NAD+Restoration+Therapy

What is The Gut-Brain Axis? An Exploration of The Communication Pathways Between The Brain, The Gut, And The Microbiota

What is The Gut-Brain Axis? An Exploration of The Communication Pathways Between The Brain, The Gut, And The Microbiota

“Key Learning Objectives:

– Understand the importance of a gut-brain communication system

– Learn about signaling pathways in the gut-brain axisLearn how the gut microbiota influences brain function

– Discover how the gut microbiota can be targeted to influence brain function

WHAT IS THE GUT-BRAIN AXIS?

The gut, its microbes, and the brain are connected by a complex communication and regulation system called the gut-brain axis. The gut-brain axis (also known as brain-gut axis, microbiota-gut-brain axis, gut-brain connection) is a bidirectional signaling network made up of neurons, hormones, immune cells, and microbial molecules.[1,2] It is part of a larger system that informs the brain of the internal state and health of our body. This sense is called interoception and it’s crucial for the maintenance of physiological balance in our body, a state known as homeostasis.[3] “

What is The Gut-Brain Axis? An Exploration of The Communication Pathways Between The Brain, The Gut, And The Microbiota
Probiotic bacteria as modulators of cellular senescence: emerging concepts and opportunities

Probiotic bacteria as modulators of cellular senescence: emerging concepts and opportunities

Probiotic bacteria are increasingly gaining importance in human nutrition owing to their multifaceted health beneficial effects. Studies have also shown that probiotic supplementation is useful in mitigating age-associated oxi-inflammatory stress, immunosenescence, and gut dysbiosis thereby promoting health and longevity. However, our current understanding of the process of aging suggests a strong interrelationship between the accumulation of senescent cells and the development of aging phenotype, including the predisposition to age-related disorders. The present review studies the documented pro-longevity effects of probiotics and highlights how these beneficial attributes of probiotics could be related to the mitigation of cellular senescence.

https://www.tandfonline.com/doi/full/10.1080/19490976.2019.1697148?af=R&utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Identification of a key protein linked to ageing

Identification of a key protein linked to ageing

“These studies demonstrate an important link between the [pathological] accelerated ageing process and normal aging, and also expose the CSB protein as a key factor against cellular ageing” concludes Dr. Ricchetti.

https://medicalxpress.com/news/2019-12-identification-key-protein-linked-ageing.html

The cyanthin diterpenoid and sest… preview & related info | Mendeley

The cyanthin diterpenoid and sest… preview & related info | Mendeley

Hericium erinaceus was used in traditional Chinese medicine for physiologically beneficial medicines. Recently, it has become a candidate in causing positive brain health-related activities. We previously reported that Hericium erinaceus mycelium ameliorates Alzheimer’s disease (AD)-related pathologies.

https://www.mendeley.com/catalogue/cyanthin-diterpenoid-sesterterpene-constituents-hericium-erinaceus-mycelium-ameliorate-alzheimers-di/

Epigenetics of aging and disease: a brief overview. – PubMed – NCBI

Epigenetics of aging and disease: a brief overview. – PubMed – NCBI

“Aging is an important risk factor for several human diseases such as cancer, cardiovascular disease and neurodegenerative disorders, resulting from a combination of genetic and environmental factors (e.g., diet, smoking, obesity and stress), which, at molecular level, cause changes in gene expression underlying the decline of physiological function. Epigenetics, which include mechanisms regulating gene expression independently of changes to DNA sequence, regulate gene expression by modulating the structure of chromatin or by regulating the binding of transcriptional machinery to DNA. Several studies showed that an impairment of epigenetic mechanisms promotes alteration of gene expression underlying several aging-related diseases. Alteration of these mechanisms is also linked with changes of gene expression that occurs during aging processes of different tissues. In this review, we will outline the potential role of epigenetics in the onset of two age-related pathologies, cancer and cardiovascular diseases.”

https://www.ncbi.nlm.nih.gov/pubmed/31811572?dopt=Abstract

Chronic inflammation in the etiology of disease across the life span. – PubMed – NCBI

Chronic inflammation in the etiology of disease across the life span. – PubMed – NCBI

Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.

https://www.ncbi.nlm.nih.gov/pubmed/31806905?dopt=Abstract

The distributions of protein coding genes within chromatin domains in relation to human disease | Epigenetics & Chromatin | Full Text

The distributions of protein coding genes within chromatin domains in relation to human disease | Epigenetics & Chromatin | Full Text

“The unprecedented resolution of genome-wide interaction maps shows functional consequences that extend the initial thought of an efficient DNA packaging mechanism: gene regulation, DNA repair, chromosomal translocations and evolutionary rearrangements seem to be only the peak of the iceberg. One key concept emerging from this research is the topologically associating domains (TADs) whose functional role in gene regulation and their association with disease is not fully untangled.”

https://epigeneticsandchromatin.biomedcentral.com/articles/10.1186/s13072-019-0317-2