Your thoughts can have a profound impact on your health

I will breath deeply for I refuse to leave my cells unoxygenated.

I will guard my  mind vigilantly when receiving a “diagnosis”.

And will use my own voice and power to make my body strong.

Be nourished by whole foods and quality supplementation.

Getting clean water and fresh air and most important sunshine.

Be away from toxic environment, places , chemicals and people.

Be surrounded by love, warmth and satisfying kisses and hugs.

Be well my friends.

Connie

logo

My scientist friend asked how to detox or clean his body from toxins

Over the years, I have experienced family and friends dying of cancer. I observed their lifestyle and toxins they are exposed to. So to answer my friend’s question on how to detox and the mechanism of cleaning our body or getting rid of toxins, I listed some items for Dos and Donts.

Our lymphatic system which travels opposite our blood is responsible for cleaning our blood.  Search for lymphatic, massage and detox in this site http://www.clubalthea.com

When we clean the many bad foods or toxins that entered our body, we must clean our liver first, our laboratory.  It is closely linked to our heart that during our last breath, our liver is the first and last signal that our heart gets to shut down.

Detox or cleaning our cells from toxins is the key to living longer, the anti-aging process we all are seeking for. In my 50s, I could have died long time ago if I was born centuries ago with no clean water, fresh produce and raising a dozen children. Each child is minus 5 years of a woman’s age.

Detox is like cleaning the toilet. The following are detox tips and anti-aging tips to clean your cells:

Dos in cleansing your body from toxin, also detoxes your liver

  • Massage
  • Adequate sleep
  • Filtered water
  • Lemon
  • Baking soda (pinch in your drinking water)
  • Activated charcoal
  • Digestive enzymes from pineapple and papaya
  • Apple cider vinegar
  • Wash produce with salt or diluted vinegar
  • No over ripe fruits and left over foods or 3-day old rice ( aflatoxin , mycotoxin )
  • No charred BBQ
  • Whole foods ; sulfur rich as they are anti-inflammatory (ginger, garlic, turmeric, coconut, walnuts)
  • Deep breathing thru nose and blow out thru mouth
  • Prayer: May God’s light energy be with you and say Amen to accept it.
  • Resveratrol from Berries, kiwi, citrus fruit
  • Fasting
  • Activated charcoal
  • Clean air

Donts are ways that when practiced or consumed can kills our nerve cells and produce toxins in our cells.

  • Avoidance of too much caffeine, iron and sugar, these are food for cancer
  • Other metal toxins
  • TRANS fat
  • Processed
  • Plastics in food
  • Stress
  • Shift work: not sleeping from 10pm to 4 am
  • Radiation
  • Over medications, chemo, other carcinogens
  • Avoid exposure to fumes, chemicals (formaldehydes,carcinogens,toxins)

 

——-

Hi Connnie,

And what is your recipe for liver detox and the mechanism by which it works to accomplish that?

From: Male friend in his late 50s whose brother died of pancreatic cancer

Why women have more Alzheimer’s disease than men

Gender and mitochondrial toxicity of amyloid-beta peptide

The main risk factors for developing Alzheimer’s disease (AD) are age and gender. The incidence of the disease is higher in women than in men, and this cannot simply be attributed to the higher longevity of women versus men. Thus, there must be a specific pathogenic mechanism to explain the higher incidence of AD cases in women.

In this regard, it is notable that mitochondria from young females are protected against amyloid-beta toxicity, generate less reactive oxygen species, and release less apoptogenic signals than those from males.

However, all this advantage is lost in mitochondria from old females. Since estrogenic compounds protect against mitochondrial toxicity of amyloid-beta, estrogenic action may be important in protecting cells from amyloid-beta toxicity and suggests a possible treatment or prevention strategy for AD. Unfortunately, to date, clinical trials with Ginkgo biloba and other estrogenic therapies have not proved successful in treating AD. As such, more experiments and clinical trials are indeed warranted to find conditions in which estrogenic compounds may be useful to prevent or treat AD.

https://www.ncbi.nlm.nih.gov/pubmed/20442496


Connie’s comments: As women age, we have experienced all kinds of stress and inflammatory substances (sugar, aspartame, toxic metals, stress, lack of whole foods, others) that can affect our predisposition to Alzheimer’s disease. The ratio of getting Alzheimer’s between women and men is 3:1.

Natural communication breakdown in aging

A naturally produced compound rewinds aspects of age-related demise in mice.

Researchers have discovered a cause of aging in mammals that may be reversible.

The essence of this finding is a series of molecular events that enable communication inside cells between the nucleus and mitochondria. As communication breaks down, aging accelerates. By administering a molecule naturally produced by the human body, scientists restored the communication network in older mice. Subsequent tissue samples showed key biological hallmarks that were comparable to those of much younger animals.

This image shows and labels the mitochondria.

“The aging process we discovered is like a married couple—when they are young, they communicate well, but over time, living in close quarters for many years, communication breaks down,” said Harvard Medical School Professor of Genetics David Sinclair, senior author on the study. “And just like with a couple, restoring communication solved the problem.”

This study was a joint project between Harvard Medical School, the National Institute on Aging, and the University of New South Wales, Sydney, Australia, where Sinclair also holds a position.

The findings are published Dec. 19 in Cell.

Communication breakdown

Mitochondria are often referred to as the cell’s “powerhouse,” generating chemical energy to carry out essential biological functions. These self-contained organelles, which live inside our cells and house their own small genomes, have long been identified as key biological players in aging. As they become increasingly dysfunctional overtime, many age-related conditions such as Alzheimer’s disease and diabetes gradually set in.

Researchers have generally been skeptical of the idea that aging can be reversed, due mainly to the prevailing theory that age-related ills are the result of mutations in mitochondrial DNA—and mutations cannot be reversed.

Sinclair and his group have been studying the fundamental science of aging—which is broadly defined as the gradual decline in function with time—for many years, primarily focusing on a group of genes called sirtuins. Previous studies from his lab showed that one of these genes, SIRT1, was activated by the compound resveratrol, which is found in grapes, red wine and certain nuts.

The is the SIRT1 protein.

Ana Gomes, a postdoctoral scientist in the Sinclair lab, had been studying mice in which this SIRT1 gene had been removed. While they accurately predicted that these mice would show signs of aging, including mitochondrial dysfunction, the researchers were surprised to find that most mitochondrial proteins coming from the cell’s nucleus were at normal levels; only those encoded by the mitochondrial genome were reduced.

“This was at odds with what the literature suggested,” said Gomes.

As Gomes and her colleagues investigated potential causes for this, they discovered an intricate cascade of events that begins with a chemical called NAD and concludes with a key molecule that shuttles information and coordinates activities between the cell’s nuclear genome and the mitochondrial genome. Cells stay healthy as long as coordination between the genomes remains fluid. SIRT1’s role is intermediary, akin to a security guard; it assures that a meddlesome molecule called HIF-1 does not interfere with communication.

For reasons still unclear, as we age, levels of the initial chemical NAD decline. Without sufficient NAD, SIRT1 loses its ability to keep tabs on HIF-1. Levels of HIF-1 escalate and begin wreaking havoc on the otherwise smooth cross-genome communication. Over time, the research team found, this loss of communication reduces the cell’s ability to make energy, and signs of aging and disease become apparent.

“This particular component of the aging process had never before been described,” said Gomes.

While the breakdown of this process causes a rapid decline in mitochondrial function, other signs of aging take longer to occur. Gomes found that by administering an endogenous compound that cells transform into NAD, she could repair the broken network and rapidly restore communication and mitochondrial function. If the compound was given early enough—prior to excessive mutation accumulation—within days, some aspects of the aging process could be reversed.

This is a diagram which shows what happens when the nucleus breaks down.

Cancer connection

Examining muscle from two-year-old mice that had been given the NAD-producing compound for just one week, the researchers looked for indicators of insulin resistance, inflammation and muscle wasting. In all three instances, tissue from the mice resembled that of six-month-old mice. In human years, this would be like a 60-year-old converting to a 20-year-old in these specific areas.

One particularly important aspect of this finding involvesHIF-1. More than just an intrusive molecule that foils communication, HIF-1 normally switches on when the body is deprived of oxygen. Otherwise, it remains silent. Cancer, however, is known to activate and hijack HIF-1. Researchers have been investigating the precise role HIF-1 plays in cancer growth.

“It’s certainly significant to find that a molecule that switches on in many cancers also switches on during aging,” said Gomes. “We’re starting to see now that the physiology of cancer is in certain ways similar to the physiology of aging. Perhaps this can explain why the greatest risk of cancer is age.”

“There’s clearly much more work to be done here, but if these results stand, then certain aspects of aging may be reversible if caught early,” said Sinclair.

The researchers are now looking at the longer-term outcomes of the NAD-producing compound in mice and how it affects the mouse as a whole. They are also exploring whether the compound can be used to safely treat rare mitochondrial diseases or more common diseases such as Type 1 and Type 2 diabetes. Longer term, Sinclair plans to test if the compound will give mice a healthier, longer life.

Notes about this neurogenetics and aging research

The Sinclair lab is funded by the National Institute on Aging (NIA/NIH), the Glenn Foundation for Medical Research, the Juvenile Diabetes Research Foundation, the United Mitochondrial Disease Foundation and a gift from the Schulak family.

Written by David Cameron
Contact: David Cameron – Harvard University
Source: Harvard University press release
Image Source: The images are credited to Ana Gomes and are adapted from the Harvard press release.
Original Research: Abstract for “Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging” by Ana P. Gomes, Nathan L. Price, Alvin J.Y. Ling, Javid J. Moslehi, Magdalene K. Montgomery, Luis Rajman, James P. White, João S. Teodoro, Christiane D. Wrann, Basil P. Hubbard, Evi M. Mercken, Carlos M. Palmeira, Rafael de Cabo, Anabela P. Rolo, Nigel Turner, Eric L. Bell, and David A. Sinclair in Cell. Published online December 19 2013 doi:10.1016/j.cell.2013.11.037


Here are four foods that are good sources of resveratrol

Red Grapes

Grapes don’t have to be fermented to contain this antioxidant. It’s actually found in the skin of red grapes along with other nutrients, such as minerals manganese and potassium and vitamins K, C and B1.

Peanut Butter

Peanut butter is great for dressing up apples and celery, but it also contains some resveratrol (up to .13 mg per cup). Peanut butter is a great source of niacin and manganese.

Dark Chocolate

In dark chocolate, resveratrol blends nicely with other antioxidants and also minerals, such as iron, copper and manganese. Who doesn’t like chocolate?

Blueberries

Blueberries don’t have quite as much resveratrol as grapes, but they are also a great source of other antioxidants, dietary fiber, vitamins C and K and manganese.


NAD

Nicotinamide adenine dinucleotide (NADH) supplements can be used by people struggling with clinical depression, those affected by Alzheimer’s disease and Parkinson’s disease as well as people with long term chronic fatigue syndrome. The beneficial effects of nicotinamide adenine dinucleotide (NADH) will best be felt after supplementation goes on for some period of time. Each patient may respond to the supplement in a different way.

Some condition specific uses of NADH are discussed below in brief.

Nicotinamide adenine dinucleotide (NADH) facilitates in providing relief from a health condition known as chronic fatigue syndrome.

The nicotinamide adenine dinucleotide (NADH) is primarily found in the foods like fish, all poultry, and cattle, and in yeast containing food products.

Though it may be a little hard to find, NADH supplements can be found in some health food stores.

Nevertheless, it is yet to be ascertained whether the body is able to effectively take up or make use of the NADH obtained from the above mentioned sources. In addition to the sources mentioned above, NADH is also available in the form of a dietary supplement.

Deficiencies and susceptibility

A deficiency of nicotinamide adenine dinucleotide (NADH) can only happen if the diet is deficient in vitamin B3, and except in long term alcoholics, deficiencies of the vitamin B3 is almost unknown in the modern western world.

Is low blood sugar genetic?

20:80 is my guess. Our genes affect us 20% of the time while our environment and lifestyle affects us 80% of the time (epigenetics).

Each person metabolize glucose or drugs or food in the liver differently. Pharmacogenetic tests classified these into 4 groups of people.

We have to choose good carbohydrates from whole foods (colored greens, fibrous whole foods) and avoid toxins (alcohol, soda, aspartame, processed foods, burned BBQ meat, etc). We sleep before 10pm and exercise 30min every day. We destress and be proactive with our own health.

In mammals the response to dietary glucose is more complex because it combines effects related to glucose metabolism itself and effects secondary to glucose-dependent hormonal modifications, mainly pancreatic stimulation of insulin secretion and inhibition of glucagon secretion. In the pancreatic β cells, glucose is the primary physiological stimulus for the regulation of insulin synthesis and secretion. In the liver, glucose, in the presence of insulin, induces expression of genes encoding glucose transporters and glycolytic and lipogenic enzymes.

Although insulin and glucagon were long known as critical in regulating gene expression, it is only recently that carbohydrates also have been shown to play a key role in transcriptional regulation. DNA sequences and DNA binding complexes involved in the glucose-regulated gene expression have been characterized recently in liver and β cells.

Regulation of gene expression by nutrients in mammals is an important mechanism allowing them to adapt to the nutritional environment.

In-vivo and in-vitro experiments have demonstrated that the transcription of genes coding for lipogenic and glycolytic enzymes in liver and/or adipose tissue is upregulated by glucose.

In order for glucose to act as a gene inducer, it must be metabolized.

blood su.JPG

Brain Metabolism Predicts Fluid Intelligence in Young Adults

A healthy brain is critical to a person’s cognitive abilities, but measuring brain health can be a complicated endeavor. A new study by University of Illinois researchers reports that healthy brain metabolism corresponds with fluid intelligence – a measure of one’s ability to solve unusual or complex problems – in young adults.

The results are reported in the journal Cerebral Cortex.

“Fluid intelligence is one of the most useful cognitive measures available,” said U. of I. Ph.D. candidate Aki Nikolaidis, who led the research with Ryan Larsen, a research scientist at the Beckman Institute for Advanced Science and Technology, and Beckman Institute director Arthur Kramer.

“This domain relates to an individual’s job satisfaction and salary level, among other real-world outcomes,” he said.

The researchers measured concentrations of the molecule N-acetyl aspartate, a known marker of metabolic activity in the brain, using magnetic resonance spectroscopy. Nikolaidis then looked at the relationship between NAA concentrations in different regions of the brain and fluid intelligence.

“MR spectroscopy allows us to go beyond simply imaging the structures of the brain. It allows us to image the capacity of the brain to produce energy,” Larsen said.

Previous research relating MR spectroscopy data to cognition has been inconsistent. One explanation may be that researchers fail to account for all relevant factors that relate to cognition, including brain size, in their analyses, Nikolaidis said. One goal of the current study was to address these previous contradictions.

“We wanted to do a more definitive study with a large sample size and with a higher quality methodological approach of acquiring the data,” Nikolaidis said. The researchers were able to create a more detailed map of NAA concentration in the brain than previous studies had, he said.

Image shows a girl reading a book.

The team found that NAA concentration in an area of the brain linked to motor abilities in the frontal and parietal cortices was specifically linked to fluid intelligence but not to other closely related cognitive abilities. The brain’s motor regions have a role in planning and visualizing movements as well as carrying them out, Nikolaidis said. Mental visualization is a key element of fluid intelligence, he said.

The researchers concluded that fluid intelligence depends on brain metabolism and health. While overall brain size is genetically determined and not readily changed, NAA levels and brain metabolism may respond to health interventions including diet, exercise or cognitive training, Nikolaidis said.

ABOUT THIS NEUROSCIENCE RESEARCH

Funding: This research was funded by the Office of Naval Research; Abbott Nutrition through the Center for Nutrition, Learning, and Memory at the U. of I.; and the National Science Foundation.

Source: Sarah Banducci – University of Illinois at Urbana Champaign
Image Source: The image is in the public domain.
Original Research: Abstract for “Multivariate Associations of Fluid Intelligence and NAA” by Aki Nikolaidis, Pauline L. Baniqued, Michael B. Kranz, Claire J. Scavuzzo, Aron K. Barbey, Arthur F. Kramer, and Ryan J. Larsen in Cerebral Cortex. Published online March 22 2016 doi:10.1093/cercor/bhw070


Multivariate Associations of Fluid Intelligence and NAA

Understanding the neural and metabolic correlates of fluid intelligence not only aids scientists in characterizing cognitive processes involved in intelligence, but it also offers insight into intervention methods to improve fluid intelligence. Here we use magnetic resonance spectroscopic imaging (MRSI) to measure N-acetyl aspartate (NAA), a biochemical marker of neural energy production and efficiency. We use principal components analysis (PCA) to examine how the distribution of NAA in the frontal and parietal lobes relates to fluid intelligence. We find that a left lateralized frontal-parietal component predicts fluid intelligence, and it does so independently of brain size, another significant predictor of fluid intelligence. These results suggest that the left motor regions play a key role in the visualization and planning necessary for spatial cognition and reasoning, and we discuss these findings in the context of the Parieto-Frontal Integration Theory of intelligence.

“Multivariate Associations of Fluid Intelligence and NAA” by Aki Nikolaidis, Pauline L. Baniqued, Michael B. Kranz, Claire J. Scavuzzo, Aron K. Barbey, Arthur F. Kramer, and Ryan J. Larsen in Cerebral Cortex. Published online March 22 2016 doi:10.1093/cercor/bhw070