Link to placental marker of prenatal stress to bran mitochondrial dysfunction

How to have healthy blood flow to your heart?

blood flowI believe that a healthy blood flow to the heart starts with clean alkaline blood processed by a healthy liver free from toxins such as drugs, alcohol and toxic medications (narcotics).  Consumption of foods rich in nutrients such as folate, Vitamin C and B and L-arginine amino acid can prevent mitochondrial damage.  Example of foods rich in these nutrients are cage-free eggs, dairy products like cultured yogurtkefir and raw cheeses (choose organic and raw dairy whenever possible) Grass-fed beef or meat and pasture-raised poultry (including turkey and chicken) Liver and organ meats (such as chicken liver pate).

And the most important factors for a healthy heart are deep cleansing breath from calm mind, sleep, stress-free and healthy lifestyle with positive energies from sunshine, massage and grounding (walking barefoot on the beach or ground).


Sun, Earth and the Human Touch — 3 Key Principles for Healthy Blood Flow

Pollack has also clearly demonstrated there are three natural energies that result in separation of charges that create flow:

1.Sunlight charges up your blood vessels, which increases the flow of blood. When the sun’s rays penetrate your skin, it causes a massive increase of nitric oxide that acts as a vasodilator. As much as 60 percent of your blood can be shunted to the surface of your skin through the action of nitric oxide. This helps absorb solar radiation, which then causes the water in your blood to capture the energy and become structured.

This is a key component for a healthy heart. The ideal is to be exposed to the sun while grounding, meaning walking barefoot. This forms a biological circuit that makes it work even better.

2.Negative ions from the Earth, also known as earthing or grounding. This also charges up your blood vessels, creates a separation of charges, creates more positive ions and allows the blood to flow upward, against gravity.

3.The field effect or touch from another living being, such as laying on of hands.

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the family of mitochondrial cytopathies, which also include MERRF, and Leber’s hereditary optic neuropathy.

Most people with MELAS have a buildup of lactic acid in their bodies, a condition called lactic acidosis. Increased acidity in the blood can lead to vomiting, abdominal pain, extreme tiredness (fatigue), muscle weakness, loss of bowel control, and difficulty breathing. Less commonly, people with MELAS may experience involuntary muscle spasms (myoclonus), impaired muscle coordination (ataxia), hearing loss, heart and kidney problems, diabetes, epilepsy, and hormonal imbalances.

MELAS is a condition that affects many of the body’s systems, particularly the brain and nervous system (encephalo-) and muscles (myopathy). In most cases, the signs and symptoms of this disorder appear in childhood following a period of normal development.[3]Early symptoms may include muscle weakness and pain, recurrent headaches, loss of appetite, vomiting, and seizures. Most affected individuals experience stroke-like episodes beginning before age 40. These episodes often involve temporary muscle weakness on one side of the body (hemiparesis), altered consciousness, vision abnormalities, seizures, and severe headaches resembling migraines. Repeated stroke-like episodes can progressively damage the brain, leading to vision loss, problems with movement, and a loss of intellectual function (dementia). The stroke-like episodes can be mis-diagnosed as epilepsy by a doctor not aware of the MELAS condition.

Patients are managed according to what areas of the body are affected at a particular time. Enzymesamino acidsantioxidants and vitamins have been used.

Also the following supplements may help:

  • CoQ10 has been helpful for some MELAS patients.[7] Nicotinamide has been used because complex l accepts electrons from NADH and ultimately transfers electrons to CoQ10.
  • Riboflavin has been reported to improve the function of a patient with complex l deficiency and the 3250T-C mutation.[8]
  • The administration of L-arginine during the acute and interictal periods may represent a potential new therapy for this syndrome to reduce brain damage due to impairment of vasodilation in intracerebral arteries due to nitric oxide depletion

Calcium, magnesium, Vitamin D3 and K2 and Omega-3s cut risk of cancer

Eat eggs, fish, pickled veggies and wholefoods from cooked/raw veggies and fruits to promote cell growth. These foods are rich in Vitamin D3 and K2.
Vitamin D3 and K2 ensures calcium in bones and not in other cells.

Cancer risks are prevalent when consuming processed meat and chemicals/drugs/medications rich in un-absorbed free calcium (CA++).

Fish Oil. Calcium, magnesium (Ca:Mg in 60:40 ratio), Vitamin D3 and K2 from whole foods and Omega-3s cut risk of metabolic syndrome and cancer. These nutrients also help improve components of metabolic syndrome and reduce risk for cardiovascular disease.

calcium 2 pluscauses of cell damage

Bioactive Compounds and Cancer – Page 449 – Google Books Result

John A. Milner, ‎Donato F. Romagnolo – 2010 – ‎Medical

Experiments show that unabsorbed calcium in the lumen of the colon can prevent the adverse effects of bile acids and free fatty acids on the epithelial cells. … The bile and fatty acids have been shown to have irritating effects and to stimulate cell proliferation, thereby promoting a variety of cell damagingeffects in the colon.

Overview of Calcium – Dietary Reference Intakes for Calcium and …

by AC Ross – ‎2011 – ‎Cited by 1 – ‎Related articles

Calcium is excreted through the feces as unabsorbed intestinal calcium and is shed in mucosal cellsand secretions including saliva, gastric juices, pancreatic juice, and bile. Endogenous fecal calciumlosses are approximately 2.1 mg/kg per day in adults and about 1.4 mg/kg per day in children (Abrams et al., 1991).

Handbook of Dairy Foods and Nutrition, Second Edition

Parathyroid hormone and 1,25-dihydroxy vitamin D are thought to increase blood pressure through increases in intracellular free calcium and in muscle tone.” These observations serve to … This increases the likelihood that the cells lining the colon will be damaged, proliferate, and progress toward cancer. Epidemiologic …

API Textbook of Medicine (Volume I & II)

YP Munjal – 2015 – ‎Medical

Iron, folic acid and calcium are preferentially absorbed in the duodenum and proximal jejunum, which are also the sites maximally affected in … due to eosinophil infiltration Mucosal damage due to bacteria-laden macrophages Epithelial cell infection with or without mucosal invasion leading to damage to villuscells, often …

Plant Physiological Ecology: Field methods and instrumentation

R. Pearcey, ‎H.A. Mooney, ‎P.W. Rundel – 2012 – ‎Science

This equilibration period also serves to rinse any unabsorbed ions out of the free space between rootcells. Next, roots are transferred for a short time (e.g. 10–20 min) to a radioactively labeled solution (containing calcium) of the nutrient being studied, then rinsed in a … First, does removing roots from soil damage them?

Calcification and Its Treatment with Magnesium and Sodium Thiosulfate…/calcification-and-its-treatment-with-magnesium-and-sodium-thiosulfat…

Dec 8, 2009 – Magnesium acts as an antioxidant against free radical damage of the mitochondria. Magnesium has been called nature’s “calcium channel blocker” because of its ability to prevent coronary artery spasm, arrhythmias, and to reduce blood pressure. “Calcium enters the cells of the heart by way of calcium …

Calcium1 | Basicmedical Key

Jul 27, 2016 – For that reason, cells must keep free calcium ion concentrations in the cytosol at extremely low levels, typically on the order of 100 nmol. This is 10,000-fold lower than the … of proteins to bind calcium. Calcification in tissues other than bones and teeth is generally a sign of tissue damageand cell death.

Chapter 11. Calcium

In the cellular compartment the total calcium concentration is comparable with that in the ECF, but thefree calcium concentration is lower by several orders of …. The unabsorbed component appears in the faeces together with the unabsorbed component of digestive juice calcium known as endogenous faecal calcium. Thus …


Whenever an electron is torn from an atom a little spark is produced that can damage cell membranes. It’s called free radical damage and can be seen under a microscope in live blood cell analysis. … Significant amount of unabsorbed calcium left in the body will interact with other inorganic compounds to form stones.

The Vitamin Combination That May Reduce Your Osteoporosis

May 16, 2012 – When you’re supplementing with calcium and vitamin D3, you must also take vitamin K2 to reduce your osteoporosis risk.

The Delicate Dance Between Vitamins D and K – Dr. Mercola

Mar 26, 2011 – According to recent findings, the benefits of vitamin D, in terms of bone strength and cardiovascular health, are greatly enhanced when combined with vitamin K. Vitamin D improves your bone health by helping you absorb calcium. However, it is vitamin K that directs calcium to your skeleton, to prevent it …

Vitamin D supplements: Are yours helping or hurting you?

Almost every expert recommends it. And everyone’s taking it. But what if we’ve been using it wrong? What if our vitamin D supplements aren’t really helping us at all? If your car’s oil light went on once a week…and every time you checked the oil, it was running low…what would you do? Shrug? Top up the oil tank (again)? …

Vitamins K1 and K2: The Emerging Group of Vitamins Required for …

by GK Schwalfenberg – ‎2017 – ‎Cited by 2 – ‎Related articles

Jun 18, 2017 – Vitamin Dcalcium, and vitamin K2 supplementation reduces undercarboxylated osteocalcin and improves lumbar bone mineral density [18]. … subjects free from myocardial infarction at baseline followed up for 7 years, the odds ratio of the highest tertile intake of menaquinone (vitaminK2) compared to the …

Proper Calcium Use: Vitamin K2 as a Promoter of Bone and …

by K Maresz – ‎2015 – ‎Cited by 18 – ‎Related articles

An increased intake of vitamin K2 could be a means of lowering calcium-associated health risks. … Women’s Health Initiative showed that those women taking 1000 mg/day in the form of calciumsupplements, with or without the addition of 400 IU/day of vitamin D, increased their risk of cardiovascular events by 15% to 22%, …

The use of calcium and vitamin D in the management of osteoporosis

by JA Sunyecz – ‎2008 – ‎Cited by 117 – ‎Related articles

Osteoporosis poses a significant public health issue, causing significant morbidity and mortality.Calcium and vitamin D utilization in the optimization of bone health is often overlooked by patients and health care providers. In addition, the optimal standard of care for osteoporosis should encompass adequate calcium and …

3 Major Benefits of Vitamin K2 For Your Heart and Bones – Dr. Jockers

New studies are looking at another subtype called vitamin K2 and its effect in synergy with Vitamin D3on various health factors. Vitamin K2 appears to be a very important nutrient … Inadequate K2 inhibits osteocalcin production and reduces calcium flow into bone tissue. This leads to reduced bone mass and a weakened …

Prevent Heart Disease with Vitamins A, D3, and K2 : Terry Talks Nutrition

And that lack of knowledge just might be slowly killing them. Vitamins A, D3, and K2 work as partners to: • Keep calcium in your bones and out of your arteries. • Prevent dangerous blood clots, heart attacks, and high blood pressure. • Help keep arteries flexible and strong. • Reduce inflammatory markers in the bloodstream.

Vitamin K2 and Atherosclerosis | LIfe Extension

In addition, subjects taking the combination of vitamins K2 and D3 showed a reduction in carotid artery calcification score in all patients except those with the highest scores at baseline.6 This indicates thatcalcium was staying in the bones, where it belongs, and out of the arteries. These results clearly indicated that vitamin …

Vitamin Code® RAW Calcium™ | Garden of Life

RAW Whole Food Plant Calcium Formula with Magnesium, Vitamins D3 & K2 (MK-7); Free from Crushed Rock, Limestone, Chalk and Animal Bones … ††Regular exercise and a healthy diet with enough calciumand vitamin D helps you maintain good bone health and may reduce the risk of osteoporosis later in life.


Alzheimer’s Drug Turns Back Clock in Powerhouse of Cell

Alzheimer’s Drug Turns Back Clock in Powerhouse of Cell

Summary: Researchers have developed a new drug that can help treat Alzheimer’s disease and has been shown to reverse aging in mice.Source: Salk Institute.

The experimental drug J147 is something of a modern elixir of life; it’s been shown to treat Alzheimer’s disease and reverse aging in mice and is almost ready for clinical trials in humans. Now, Salk scientists have solved the puzzle of what, exactly, J147 does. In a paper published January 7, 2018, in the journal Aging Cell, they report that the drug binds to a protein found in mitochondria, the energy-generating powerhouses of cells. In turn, they showed, it makes aging cells, mice and flies appear more youthful.

“This really glues together everything we know about J147 in terms of the link between aging and Alzheimer’s,” says Dave Schubert, head of Salk’s Cellular Neurobiology Laboratory and the senior author on the new paper. “Finding the target of J147 was also absolutely critical in terms of moving forward with clinical trials.”

Schubert’s group developed J147 in 2011, after screening for compounds from plants with an ability to reverse the cellular and molecular signs of aging in the brain. J147 is a modified version of a molecule found in the curry spice curcumin. In the years since, the researchers have shown that the compound reverses memory deficits, potentiates the production of new brain cells, and slows or reverses Alzheimer’s progression in mice. However, they didn’t know how J147 worked at the molecular level.

test tube

In the new work, led by Schubert and Salk Research Associate Josh Goldberg, the team used several approaches to home in on what J147 is doing. They identified the molecular target of J147 as a mitochondrial protein called ATP synthase that helps generate ATP–the cell’s energy currency–within mitochondria. They showed that by manipulating its activity, they could protect neuronal cells from multiple toxicities associated with the aging brain. Moreover, ATP synthase has already been shown to control aging in C. elegans worms and flies.

“We know that age is the single greatest contributing factor to Alzheimer’s, so it is not surprising that we found a drug target that’s also been implicated in aging,” says Goldberg, the paper’s first author.

Further experiments revealed that modulating activity of ATP synthase with J147 changes the levels of a number of other molecules–including levels of ATP itself–and leads to healthier, more stable mitochondria throughout aging and in disease.

“I was very surprised when we started doing experiments with how big of an effect we saw,” says Schubert. “We can give this to old mice and it really elicits profound changes to make these mice look younger at a cellular and molecular level.”

The results, the researchers say, are not only encouraging for moving the drug forward as an Alzheimer’s treatment, but also suggest that J147 may be useful in other age-associated diseases as well.

“People have always thought that you need separate drugs for Alzheimer’s, Parkinson’s, and stroke” says Schubert. “But it may be that by targeting aging we can treat or slow down many pathological conditions that are old age-associated.”

The team is already performing additional studies on the molecules that are altered by J147’s effect on the mitochondrial ATP synthase–which could themselves be new drug targets. J147 has completed the FDA-required toxicology testing in animals, and funds are being sought to initiate phase 1 clinical trials in humans.


Source: Salk Institute
Publisher: Organized by
Image Source: image is credited to Salk Institute.
Original Research: Full open access research for “The mitochondrial ATP synthase is a shared drug target for aging and dementia” by Joshua Goldberg, Antonio Currais, Marguerite Prior, Wolfgang Fischer, Chandramouli Chiruta, Eric Ratliff, Daniel Daugherty, Richard Dargusch, Kim Finley, Pau B. Esparza-Moltó, José M. Cuezva, Pamela Maher, Michael Petrascheck and David Schubert in Aging Cell. Published online January 7 2018 doi:10.1111/acel.12715

Salk Institute “Alzheimer’s Drug Turns Back Clock in Powerhouse of Cell.” NeuroscienceNews. NeuroscienceNews, 9 January 2018.


The mitochondrial ATP synthase is a shared drug target for aging and dementia

Aging is a major driving force underlying dementia, such as that caused by Alzheimer’s disease (AD). While the idea of targeting aging as a therapeutic strategy is not new, it remains unclear how closely aging and age-associated diseases are coupled at the molecular level. Here, we discover a novel molecular link between aging and dementia through the identification of the molecular target for the AD drug candidate J147. J147 was developed using a series of phenotypic screening assays mimicking disease toxicities associated with the aging brain. We have previously demonstrated the therapeutic efficacy of J147 in several mouse models of AD. Here, we identify the mitochondrial α-F1-ATP synthase (ATP5A) as a target for J147. By targeting ATP synthase, J147 causes an increase in intracellular calcium leading to sustained calcium/calmodulin-dependent protein kinase kinase β (CAMKK2)-dependent activation of the AMPK/mTOR pathway, a canonical longevity mechanism. Accordingly, modulation of mitochondrial processes by J147 prevents age-associated drift of the hippocampal transcriptome and plasma metabolome in mice and extends lifespan in drosophila. Our results link aging and age-associated dementia through ATP synthase, a molecular drug target that can potentially be exploited for the suppression of both. These findings demonstrate that novel screens for new AD drug candidates identify compounds that act on established aging pathways, suggesting an unexpectedly close molecular relationship between the two.

“The mitochondrial ATP synthase is a shared drug target for aging and dementia” by Joshua Goldberg, Antonio Currais, Marguerite Prior, Wolfgang Fischer, Chandramouli Chiruta, Eric Ratliff, Daniel Daugherty, Richard Dargusch, Kim Finley, Pau B. Esparza-Moltó, José M. Cuezva, Pamela Maher, Michael Petrascheck and David Schubert in Aging Cell. Published online January 7 2018 doi:10.1111/acel.12715

Healthy Mitochondria Could Stop Alzheimer’s

Healthy Mitochondria Could Stop Alzheimer’s

Summary: Boosting mitochondria may defend against a form of protein stress that can reduce the formation of amyloid plaques, EPFL researchers report.

Source: EPFL.

Alzheimer’s disease is the most common form of dementia and neurodegeneration worldwide. A major hallmark of the disease is the accumulation of toxic plaques in the brain, formed by the abnormal aggregation of a protein called beta-amyloid inside neurons.

Still without cure, Alzheimer’s poses a significant burden on public health systems. Most treatments focus on reducing the formation of amyloid plaques, but these approaches have been inconclusive. As a result, scientists are now searching for alternative treatment strategies, one of which is to consider Alzheimer’s as a metabolic disease.

Taking this line of thought, Johan Auwerx’s lab at EPFL looked at mitochondria, which are the energy-producing powerhouses of cells, and thus central in metabolism. Using worms and mice as models, they discovered that boosting mitochondria defends against a particular form of protein stress, enables them to not only protect themselves, but to also reduce the formation of amyloid plaques.

Image shows a brain scan.

During normal aging and age-associated diseases such as Alzheimer’s, cells face increasing damage and struggle to protect and replace dysfunctional mitochondria. Since mitochondria provide energy to brain cells, leaving them unprotected in Alzheimer’s disease favors brain damage, giving rise to symptoms like memory loss over the years.

The scientists identified two mechanisms that control the quality of mitochondria: First, the “mitochondrial unfolded protein response” (UPRmt), which protects mitochondria from stress stimuli. Second, mitophagy, a process that recycles defective mitochondria. Both these mechanisms are the key to delaying or preventing excessive mitochondrial damage during disease.

While we have known for a while that mitochondria are dysfunctional in the brains of Alzheimer’s patients, this is the first evidence that they actually try to fight the disease by boosting quality control pathways. “These defense and recycle pathways of the mitochondria are essential in organisms, from the worm C. elegans all the way to humans,” says Vincenzo Sorrentino, first author of the paper. “So we decided to pharmacologically activate them.”

The team started by testing well-established compounds, such as the antibiotic doxycycline and the vitamin nicotinamide riboside (NR), which can turn on the UPRmt and mitophagy defense systems in a worm model (C. elegans) of Alzheimer’s disease. The health, performance and lifespan of worms exposed to the drugs increased remarkably compared with untreated worms. Plaque formation was also significantly reduced in the treated animals.

And most significantly, the scientists observed similar improvements when they turned on the same mitochondrial defense pathways in cultured human neuronal cells, using the same drugs.

The encouraging results led the researchers to test NR in a mouse model of Alzheimer’s disease. Just like C. elegans, the mice saw a significant improvement of mitochondrial function and a reduction in the number of amyloid plaques. But most importantly, the scientists observed a striking normalization of the cognitive function in the mice. This has tremendous implications from a clinical perspective.

According to Johan Auwerx, tackling Alzheimer’s through mitochondria could make all the difference. “So far, Alzheimer’s disease has been considered to be mostly the consequence of the accumulation of amyloid plaques in the brain,” he says. “We have shown that restoring mitochondrial health reduces plaque formation – but, above all, it also improves brain function, which is the ultimate objective of all Alzheimer’s researchers and patients.”

The strategy provides a novel therapeutic approach to slow down the progression of neurodegeneration in Alzheimer’s disease, and possibly even in other disorders such as Parkinson’s disease, which is also characterized by profound mitochondrial and metabolic defects.

The approach remains to be tested in human patients. “By targeting mitochondria, NR and other molecules that stimulate their ‘defense and recycle’ systems could perhaps succeed where so many drugs, most of which aim to decrease amyloid plaque formation, have failed,” says Vincenzo Sorrentino.


Researchers from Michigan State Uniersity also participated in this research.

Funding: Funding provided by EPFL Fellows’ Program, Associazione Italiana per la Ricerca sul Cancro, National Institutes of Health, Systems X, Velux Stiftung, Jebsen Foundation.

Source: Nik Papageorgiou – EPFL
Publisher: Organized by
Image Source: image is credited to Vincenzo Sorrentino, Mario Romani, Francesca Potenza/EPFL.
Original Research:Abstract for “Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity” by Vincenzo Sorrentino, Mario Romani, Laurent Mouchiroud, John S. Beck, Hongbo Zhang, Davide D’ Amico, Norman Moullan, Francesca Potenza, Adrien W. Schmid, Solène Rietsch, Scott E. Counts & Johan Auwerx in Nature. Published online December 6 2017 doi:10.1038/nature25143

EPFL “Healthy Mitochondria Could Stop Alzheimer’s.” NeuroscienceNews. NeuroscienceNews, 6 December 2017.


Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity

Alzheimer’s disease is a common and devastating disease characterized by aggregation of the amyloid-β peptide. However, we know relatively little about the underlying molecular mechanisms or how to treat patients with Alzheimer’s disease. Here we provide bioinformatic and experimental evidence of a conserved mitochondrial stress response signature present in diseases involving amyloid-β proteotoxicity in human, mouse and Caenorhabditis elegans that involves the mitochondrial unfolded protein response and mitophagy pathways. Using a worm model of amyloid-β proteotoxicity, GMC101, we recapitulated mitochondrial features and confirmed that the induction of this mitochondrial stress response was essential for the maintenance of mitochondrial proteostasis and health. Notably, increasing mitochondrial proteostasis by pharmacologically and genetically targeting mitochondrial translation and mitophagy increases the fitness and lifespan of GMC101 worms and reduces amyloid aggregation in cells, worms and in transgenic mouse models of Alzheimer’s disease. Our data support the relevance of enhancing mitochondrial proteostasis to delay amyloid-β proteotoxic diseases, such as Alzheimer’s disease.

“Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity” by Vincenzo Sorrentino, Mario Romani, Laurent Mouchiroud, John S. Beck, Hongbo Zhang, Davide D’ Amico, Norman Moullan, Francesca Potenza, Adrien W. Schmid, Solène Rietsch, Scott E. Counts & Johan Auwerx in Nature. Published online December 6 2017 doi:10.1038/nature25143

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Paternal exposure to environmental chemical stress affects male offspring’s hepatic mitochondria

Paternal exposure to environmental chemical stress affects male offspring’s hepatic mitochondria

Toxicological Sciences, kfx246,


Pre-conceptional paternal exposures may affect offspring’s health, which cannot be explained by mutations in germ cells, but by persistent changes in the regulation of gene expression. Therefore, we investigated whether pre-conceptional paternal exposure to benzo[a]pyrene (B[a]P) could alter the offspring’s phenotype. Male C57BL/6 mice were exposed to B[a]P by gavage for 6 weeks, 3x per week, and were crossed with unexposed BALB-c females 6 weeks after the final exposure.

The offspring was kept under normal feeding conditions and was sacrificed at 3 weeks of age. Analysis of the liver proteome by 2D-gel electrophoresis and mass spectrometry indicated that proteins involved in mitochondrial function were significantly down-regulated in the offspring of exposed fathers.

This down-regulation of mitochondrial proteins was paralleled by a reduction in mitochondrial DNA copy number and reduced activity of citrate synthase and β−hydroxyacyl-CoA dehydrogenase, but in male offspring only.

Surprisingly, analysis of hepatic mRNA expression revealed a male-specific up-regulation of the genes, whose proteins were down-regulated, including Aldh2 and Ogg1. This discrepancy could be related to several selected miRNA’s that regulate the translation of these proteins; miRNA-122, miRNA-129-2-5p and miRNA-1941 were upregulated in a gender-specific manner.

Since mitochondria are thought to be a source of intracellular reactive oxygen species, we additionally assessed oxidatively-induced DNA damage. Both 8-hydroxy-deoxyguanosine and malondialdehyde-dG adduct levels were significantly reduced in male offspring of exposed fathers.

In conclusion, we show that paternal exposure to B[a]P can regulate mitochondrial metabolism in offspring, which may have profound implications for our understanding of health and disease risk inherited from fathers.

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