Watery Diarrhea from virus/bacteria

Acute Diarrhea. Most cases of acute, watery diarrhea are caused byviruses (viral gastroenteritis). The most common ones in children are rotavirus and in adults are norovirus (this is sometimes called “cruise ship diarrhea” due to well publicized epidemics). Bacteria are a common cause of traveler’s diarrhea.

By Dr Blanca Ochoa

Acute diarrhea is one of the most commonly reported illnesses in the United States, second only to respiratory infections. Worldwide, it is a leading cause of mortality in children younger than four years old, especially in the developing world. Diarrhea that lasts less than 2 weeks is termed acute diarrhea. Persistent diarrhea lasts between 2 and 4 weeks. Chronic diarrhea lasts longer than 4 weeks.Symptoms

Diarrheal stools are those that take shape of the container, so they are often described as loose or watery. Some people consider diarrhea as an increase in the number of stools, but stool consistency is really the hallmark. Associated symptoms can include abdominal cramps fever, nausea, vomiting, fatigue and urgency. Chronic diarrhea can be accompanied by weight loss, malnutrition, abdominal pain or other symptoms of the underling illness. Clues for organic disease are weight loss, diarrhea that wakes you up at night, or blood in the stools. These are signs that your doctor will want to do a thorough evaluation to determine the cause of your symptoms. Also tell your doctor if you have a family history of celiac disease, inflammatory bowel disease (IBD), have unintentional weight loss, fever, abdominal cramping or decreased appetite. Tell your doctor if you experience bulky, greasy or very bad smelling stools.

Causes – Acute Diarrhea

Most cases of acute, watery diarrhea are caused by viruses (viral gastroenteritis). The most common ones in children are rotavirus and in adults are norovirus (this is sometimes called “cruise ship diarrhea” due to well publicized epidemics). Bacteria are a common cause of traveler’s diarrhea.

Causes – Chronic Diarrhea

Chronic diarrhea is classified as fatty or malabsorption, inflammatory or most commonly watery. Chronic bloody diarrhea may be due to inflammatory bowel disease (IBD), which is ulcerative colitis or Crohn’s disease. Other less common causes include ischemia of the gut, infections, radiation therapy and colon cancer or polyps. Infections leading to chronic diarrhea are uncommon, with the exception of parasites.

The two major causes of fatty or malabsorptive diarrhea are impaired digestion of fats due to low pancreatic enzyme levels and impaired absorption of fats due to small bowel disease. These conditions interfere with the normal processing of fats in the diet. The former is usually due to chronic pancreatitis which is a result of chronic injury to the pancreas. Alcohol damage to the pancreas is the most common cause of chronic pancreatitis in the United States. Other causes of chronic pancreatitis include cystic fibrosis, hereditary pancreatitis, trauma to the pancreas and pancreatic cancer.

The most common small bowel disease in the U.S. is celiac disease, also called celiac sprue. Crohn’s disease can also involve the small bowel. Whipple’s disease, tropical sprue, and eosinophilic gastroenteritis are some of the rare conditions that can lead to malabsorption diarrhea.

There are many causes of watery diarrhea, including carbohydrate malabsorption such as lactose, sorbitol, and fructose intolerance. Symptoms of abdominal bloating and excessive gas after consuming dairy products suggests lactose intolerance. This condition is more common in African-Americans and Asian-Americans. Certain soft drinks, juices, dried fruits and gums contain sorbitol and fructose, which can lead to watery diarrhea in people with sorbitol and fructose intolerance. Diarrhea is a frequent side effect of antibiotics. Certain other medications such as NSAIDs, antacids, antihypertensives, antibiotics and antiarrhythmics can have side effects leading to diarrhea.

Parasitic intestinal infections such as giardiasis can cause chronic diarrhea. Diabetes mellitus may be associated with diarrhea due to nerve damage and bacterial overgrowth; this occurs mainly in patients with long-standing, poorly-controlled diabetes.

Irritable bowel syndrome (IBS) is a condition often associated with diarrhea, constipation or more frequently alternating diarrhea and constipation. Other common symptoms are bloating, abdominal pain relieved with defecation and a sense of incomplete evacuation.

Risk Factors

Exposure to infectious agents is the major risk factor for acute diarrhea. Bacteria and viruses are often transmitted by the fecal-oral route, so hand washing and hygiene are important to prevent infection. Soap and water are better because alcohol-based hand sanitizers may not kill viruses. Medications such as antibiotics and drugs that contain magnesium products are also common offenders. Recent dietary changes can also lead to acute diarrhea. These including intake of coffee, tea, colas, dietetic foods, gums or mints that contain poorly absorbable sugars. Acute bloody diarrhea suggests a bacterial cause like Campylobacter, Salmonella or Shigella or Shiga-toxin E. coli. Traveler’s diarrhea is common in those who travel to developing countries and results from exposure to bacterial pathogens most commonly enterotoxigenic E. coli. The best method of prevention is to avoid eating and drinking contaminated or raw foods and beverages.


Most episodes of acute diarrhea resolve quickly without antibiotic therapy and with simple dietary modifications. See a doctor if you feel ill, have bloody diarrhea, severe abdominal pain or diarrhea lasting more than 48 hours. In patients with mild acute diarrhea, no laboratory evaluation is needed because the illness generally resolves quickly. Your doctor may perform stool tests for bacteria and parasites if your diarrhea is severe or bloody or if you traveled to an area where infections are common. If you have severe diarrhea, blood tests will be helpful to guide replacement of fluid and electrolytes and minerals such as magnesium, potassium and zinc that can become depleted.

If you have chronic diarrhea, your doctor will want to further assess etiologic factors or complications of diarrhea by obtaining several tests. These can include a blood count to look for anemia and infections, an electrolyte and kidney function panel to assess for electrolyte abnormalities and renal insufficiency, and albumin to assess your nutritional status.

A stool sample may help define the type of diarrhea. The presence of fat, microscopic amounts of blood, and white blood cells will help determine if a fatty, inflammatory, or watery diarrhea is present. A bacterial culture and ova/parasite studies of a stool specimen will also help determine if an infectious etiology is present.

Endoscopic examination of the colon with flexible sigmoidoscopy or colonoscopy and upper endoscopy are helpful in detecting the etiology of chronic diarrhea, as this allows direct examination of the bowel mucosa and the ability to obtain biopsies for microscopic evaluation. Double-balloon enteroscopy and capsule endoscopy are sometimes used to examine the mucosa of the small intestine that lies beyond the reach of conventional endoscopes.

Radiographic studies such as an upper GI series or barium enema are not routinely performed in the evaluation of chronic diarrhea, and have largely been replaced by cross-sectional imaging. Ultrasound and CT scan of the abdomen can be helpful to evaluate the bowel, pancreas and other intra-abdominal organs.

Treating Acute Diarrhea

It is important to take plenty of fluid with sugar and salt to avoid dehydration. Salt and sugar together in a beverage help your intestine absorb fluids. Milk and dairy products should be avoided for 24 to 48 hours as they can make diarrhea worse. Initial dietary choices when refeeding should begin with soups and broth.

Anti-diarrheal drug therapy can be helpful to control severe symptoms, and includes bismuth subsalicylate and antimotility agents such as loperamide. These, however, should be avoided in people with high fever or bloody diarrhea as they can worsen severe colon infections and in children because the use of anti-diarrheals can lead to complications of hemolytic uremic syndrome in cases of Shiga-toxin E. coli (E. coli 0157:H7).

Your doctor may prescribe antibiotics if you have high fever, dysentery, or moderate to severe traveler’s diarrhea. Some infections such as Shigella always require antibiotic therapy.

Treatment of chronic diarrhea depends on the etiology of the chronic diarrhea. Often, empiric treatment can be provided for symptomatic relief, when a specific diagnosis is not reached, or when a diagnosis that is not specifically treatable is reached.

Antimotility agents such as loperamide are the most effective agents for the treatment of chronic diarrhea. They reduce symptoms as well as stool weight. Attention should be paid to replacing any mineral and vitamin deficiencies, especially calcium, potassium, magnesium and zinc.


Good fats, SCFA – short chain fatty acids

This slideshow requires JavaScript.

Dietary relevance

Short-chain fatty acids are produced when dietary fiber is fermented in the colon.[5]

Short-chain fatty acids and medium-chain fatty acids are primarily absorbed through the portal vein during lipid digestion,[6] while long-chain fatty acids are packed into chylomicrons and enter lymphatic capillaries, and enter the blood first at the subclavian vein.

Medical relevance

For more details on this topic, see Butyric acid § Research.

The short-chain fatty acid butyrate is particularly important for colon health because it is the primary energy source for colonic cells and has anti-carcinogenic as well as anti-inflammatory properties[7] that are important for keeping colon cells healthy.[8][9] Butyrate inhibits the growth and proliferation of tumor cell lines in vitro, induces differentiation of tumor cells, producing a phenotype similar to that of the normal mature cell,[10] and induces apoptosis or programmed cell death of human colorectal cancer cells.[11][12] Butyrate inhibits angiogenesis by inactivating Sp1 transcription factor activity and downregulating VEGF gene expression.

Nutrient-Drug Interactions

By Adrienne Youdim, MD, FACP

Nutrition can affect the body’s response to drugs; conversely, drugs can affect the body’s nutrition.


Foods can enhance, delay, or decrease drug absorption. Foods impair absorption of many antibiotics. They can alter metabolism of drugs; eg, high-protein diets can accelerate metabolism of certain drugs by stimulating cytochrome P-450. Eating grapefruit can inhibit cytochrome P-450 34A, slowing metabolism of some drugs (eg, amiodarone, carbamazepine, cyclosporine, certain calcium channel blockers). Diets that alter the bacterial flora may markedly affect the overall metabolism of certain drugs.


Some foods affect the body’s response to drugs. For example, tyramine, a component of cheese and a potent vasoconstrictor, can cause hypertensive crisis in some patients who take monoamine oxidase inhibitors and eat cheese.


Nutritional deficiencies can affect drug absorption and metabolism. Severe energy and protein deficiencies reduce enzyme tissue concentrations and may impair the response to drugs by reducing absorption or protein binding and causing liver dysfunction. Changes in the GI tract can impair absorption and affect the response to a drug. Deficiency of calcium, magnesium, or zinc may impair drug metabolism. Vitamin C deficiency decreases activity of drug-metabolizing enzymes, especially in the elderly.


Many drugs affect appetite, food absorption, and tissue metabolism (see Table: Effects of Some Drugs on Appetite, Food Absorption, and Metabolism). Some drugs (eg, metoclopramide) increase GI motility, decreasing food absorption. Other drugs (eg, opioids, anticholinergics) decrease GI motility. Some drugs are better tolerated if taken with food.

Effects of Some Drugs on Appetite, Food Absorption, and Metabolism



Increases appetite

Alcohol, antihistamines, corticosteroids, dronabinol, insulin, megestrolacetate, mirtazapine, many psychoactive drugs, sulfonylureas, thyroid hormone

Decreases appetite

Antibiotics, bulk agents (methylcellulose, guar gum), cyclophosphamide, digoxin, glucagon, indomethacin, morphine, fluoxetine

Decreases absorption of fats


Increases blood glucose levels

Octreotide, opioids, phenothiazines, phenytoin, probenecid, thiazide diuretics, corticosteroids, warfarin

Decreases blood glucose levels

ACE inhibitors, aspirin, barbiturates, beta-blockers, insulin, monoamine oxidase inhibitors (MAOIs), oral antihyperglycemic drugs, phenacetin, phenylbutazone, sulfonamides

Decreases blood lipid levels

Aspirin and p -aminosalicylic acid, lasparaginase, chlortetracycline, colchicine, dextrans, glucagon, niacin, phenindione, statins, sulfinpyrazone, trifluperidol

Increases blood lipid levels

Adrenal corticosteroids, chlorpromazine, ethanol, growth hormone, oral contraceptives (estrogen-progestin type), thiouracil, vitamin D

Decreases protein metabolism

Chloramphenicol, tetracycline

Certain drugs affect mineral metabolism (see Table: Possible Effects of Drugs on Mineral Metabolism). Certain antibiotics (eg, tetracyclines) reduce iron absorption, as can certain foods (eg, vegetables, tea, bran).

Possible Effects of Drugs on Mineral Metabolism



Diuretics, especially thiazides, and corticosteroids

Can deplete body potassium*

Laxatives if used repeatedly

May deplete potassium*

Cortisol, desoxycorticosterone, and aldosterone

Cause marked sodium and water retention, at least temporarily

Sulfonylureas and lithium

Impair uptake or release of iodine by the thyroid

Oral contraceptives

Lower blood zinc levels, increase copper levels

Certain antibiotics (eg, tetracyclines)

Reduce iron absorption

*Depletion of potassium increases susceptibility to digoxin-induced cardiac arrhythmias.

Retention of sodium and water is much less with prednisone, prednisolone, and some other corticosteroid analogs.

Certain drugs affect vitamin absorption or metabolism (see Table: Possible Effects of Drugs on Vitamin Absorption or Metabolism).

Possible Effects of Drugs on Vitamin Absorption or Metabolism




Impairs thiamin utilization


Interferes with niacin and pyridoxine metabolism

Ethanol and oral contraceptives

Inhibit folate absorption

Phenytoin, phenobarbital, primidone, or phenothiazines

In most patients, cause folate (folic acid) deficiency*, probably because hepatic microsomal drug-metabolizing enzymes are affected


Can cause vitamin D deficiency

Aminosalicylic acid, slow-release potassium iodide, colchicine, trifluoperazine,metformin, ethanol, and oral contraceptives

Interfere with absorption of vitamin B12

Oral contraceptives with a high progestin dose .

Can cause depression, probably because of metabolically induced tryptophan deficiency

Proton pump inhibitors

Can cause deficiencies of vitamin B12, vitamin C, iron, calcium, and magnesium

*Folate supplements may make phenytoin less effective.


Alzheimer’s Disease Risk Factor Formula

ad genes.JPGAlzheimer’s Risk Factor, formula by Connie Dello Buono , ©12Sept2016

Assumption: Female, over 60yrs of age, on western diet, lives in Northern hemisphere, have families with cancer, diabetes and dementia, prone to allergies (lack zinc), digestive disorders, high dairy and sugar consumption (low magnesium and calcium,iron) and had used some medications in the past

Alzheimer’s Disease (AD) Factor = Blood sugar (0.2) + Blood Pressure (0.2) + Hard cheese and pork consumption (0.1) + Exercise and sun exposure (0.1) + number of medications (0.1) + stress level and brain concussions (0.1) + exposure to copper,fungus,molds,toxins (0.1) + genes (0.1)

  • AD Factor =1.0 (High)
  • AD Factor = <0.8 (Medium)
  • AD Factor = <0.5 (Low)

Please email your entries to motherhealth@gmail.com to create a database and get health data insights about Alzheimer’s disease. The link below contains the table in Microsoft Word. This data will also be used to track cancer, diabetes, lung disease, depression, mental health and heart disease.

Modified Alzheimer’s disease risk factor

Male = 0.05
Female =0.1
Age > 55yrs=0.1
< 55yrs = 0.05
Blood sugar
Normal/low =0

High = 0.1
Med =0.05

Blood Pressure
High = 0.1
Med =0.05
Exposure to copper,fungus,molds,toxins, smoking,alcohol,narcotics, aluminum, air pollution, medications > 5
(H,M,L)  0.2 = H,M = 0.1
Metabolic and diet:
Diabetes 0.1
Exercise and sun exposure, 3x per week = 0
No exercise = 0.1
0.1 (combo of these genes) –
Aβ42 ;  presenilin 1 & 2 ; APP ;  CASS4  CELF1  FERMT2
EPHA1, and CD2AP
Weak immune and metabolic system:
Infection and allergy 0.1


Stress level and brain concussions (H,M,L)
H = 0.1




Join 25,000 people in helping redefine health with health concierge and precision medicine.




Hypocretin, Insomia or Sleep Disturbances, Narcolepsy, Depression and Parkinson’s

Drowsy Driving

Driving and feeling sleepy. Repetitive tasks make you sleepy because you already lack sleep. You have taken your calcium and magnesium and melatonin and the bedroom has cool environment. Still, you have worries and you keep tossing back and forth on your bed. You cannot get the more than 5 hrs sleep. Your regular sleep hours are from 12midnight to 5pm and you cannot seem to add 1 more hour to it. You have a busy day and are driven to perform more and bring work at home.

What is the root cause of insomnia, narcolepsy, depression and Parkinson?

Is it because of poor muscle tone, cataplexy?

Is it because of alcohol, lifestyle, work shift pattern, caffeine, use of sedating medication, anxiety or problems or age?

The root cause if hyprocretin, a brain chemical. Eat happy foods/omega 3 such as yams, eggs, bananas, dates, cherries, hummus, a little MSG in Asian dish and fish. Avoid sugar and eat more fermented veggies (prebiotics and probiotics). Do weight bearing exercise and work in getting more sleep.

If your bedtime is 12midnight, try to calm down by 11pm (repetitive tasks-repetitive prayers/counting – leaving your worries away, no TV light, dim light, cool air, relax).


What is narcolepsy?

Narcolepsy is a chronic neurological disorder involving the loss of the brain’s ability to regulate sleep-wake cycles.[1] Symptoms include excessive daytime sleepiness, comparable to how people who do not have narcolepsy feel after 24–48 hours of sleep deprivation,[2] as well as disturbed sleep which often is confused with insomnia. Another common symptom of narcolepsy is cataplexy, a sudden and transient episode of muscle weakness accompanied by full conscious awareness, typically (though not necessarily) triggered by emotions such as laughing, crying, terror, etc.[3] affecting roughly 70% of people who have narcolepsy.[4]

The system which regulates sleep, arousal, and transitions between these states in humans is composed of three interconnected subsystems: the orexin projections from the lateral hypothalamus, the reticular activating system, and the ventrolateral preoptic nucleus.[5] In narcoleptic individuals, these systems are all associated with impairments due to a greatly reduced number of hypothalamic orexin projection neurons and significantly fewer orexin neuropeptides in cerebrospinal fluid and neural tissue, compared to non-narcoleptic individuals.[5] Those with narcolepsy generally experience the REM stage of sleep within five minutes of falling asleep, while people who do not have narcolepsy (unless they are significantly sleep deprived)[6] do not experience REM until after a period of slow-wave sleep, which lasts for about the first hour or so of a sleep cycle.

Hpocretin or Orexin, is a neuropeptide that regulates arousal, wakefulness, and appetite.

The most common form of narcolepsy, in which the sufferer briefly loses muscle tone (cataplexy), is caused by a lack of orexin in the brain due to destruction of the cells that produce it.[2]

Cataplexy is a sudden and transient episode of muscle weakness accompanied by full conscious awareness, typically triggered by emotions such as laughing, crying, or terror.[1] It is the cardinal symptom of narcolepsy with cataplexy affecting roughly 70% of people who have narcolepsy,[2] and is caused by an autoimmune destruction of the neurotransmitter hypocretin (also called orexin), which regulates arousal and wakefulness.

There are approximately 70,000 orexin producing neurons in the human brain that project from the lateral hypothalamus to neurons and brain regions that modulate wakefulness.[1][2] However, the axons from these neurons extend throughout the entire brain and spinal cord,[3] where there are also receptors for orexin.

Orexin was discovered in 1998 almost simultaneously by two independent groups of rat-brain researchers.[4][5] One group named it orexin, from orexis, meaning “appetite” in Greek; the other group named it hypocretin, because it is produced in the hypothalamus and bears a weak resemblance to secretin, another peptide.

Link Between Parkinson’s And Narcolepsy Discovered Parkinson’s disease

Link Between Parkinson’s And Narcolepsy Discovered Parkinson’s disease is well-known for its progression of motor disorders: stiffness, slowness, tremors, difficulties walking and talking. Less well known is that Parkinson’s shares other symptoms with narcolepsy, a sleep disorder characterized by sudden and uncontrollable episodes of deep sleep, severe fatigue and general sleep disorder.

Now a team of UCLA and Veterans Affairs researchers think they know why — the two disorders share something in common: Parkinson’s disease patients have severe damage to the same small group of neurons whose loss causes narcolepsy. The findings suggest a different clinical course of treatment for people suffering with Parkinson’s that may ameliorate their sleep symptoms.

In their report in the May issue of the journal Brain, Jerry Siegel, professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA, assistant resident neurobiologist Thomas C. Thannickal and associate research physiologist Yuan-Yang Lai have determined that Parkinson’s disease patients have a loss of up to 60 percent of brain cells containing the peptide hypocretin.

In 2000, this same group of UCLA researchers first identified the cause of narcolepsy as a loss of hypocretin, thought to be important in regulating the sleep cycle. This latest research points to a common cause for the sleep disorders associated with these two diseases and suggests that treatment of Parkinson’s disease patients with hypocretin or hypocretin analogs may reverse these symptoms.

More than 1 million people in the U.S. have been diagnosed with Parkinson’s disease, and approximately 20 million worldwide. (The percentage of those afflicted increases with age.) Narcolepsy affects approximately one in 2,000 individuals — about 150,000 in the United States and 3 million worldwide. Its main symptoms are sleep attacks, nighttime sleeplessness and cataplexy, the sudden loss of skeletal muscle tone without loss of consciousness; that is, although the person cannot talk or move, they are otherwise in a state of high alertness, feeling, hearing and remembering everything that is going on around them.

“When we think of Parkinson’s, the first thing that comes to mind are the motor disorders associated with it,” said Siegel, who is also chief of neurobiology research at the Sepulveda Veterans Affairs Medical Center in Mission Hills, Calif. “But sleep disruption is a major problem in Parkinson’s, often more disturbing than its motor symptoms. And most Parkinson’s patients have daytime sleep attacks that resemble narcoleptic sleep attacks.”

In fact, said Siegel, Parkinson’s disease is often preceded and accompanied by daytime sleep attacks, nocturnal insomnia, REM sleep disorder, hallucinations and depression. All of these symptoms are also present in narcolepsy.

In the study, the researchers examined 16 human brains from cadavers — five from normal adults and 11 in various stages of Parkinson’s — and found an increasing loss of hypocretin cells (Hcrt) with disease progression. In fact, said Siegel, the later stages of Parkinson’s were “characterized by a massive loss of the Hcrt neurons. That leads us to believe the loss of Hcrt cells may be a cause of the narcolepsy-like symptoms of [Parkinson’s].


From Dr Mercola:

The brain chemical hypocretin, a neurotransmitter that helps keep you awake, is most widely known for its role in the sleeping disorder known as narcolepsy.

Narcoleptics, who uncontrollably fall asleep during the day and have much higher rates of depression than the general population, are unable to produce hypocretin. This not only interferes with their sleep-wake cycle, but also may also disrupt their emotional state – a new finding that has implications for everyone.

Hypocretin May Regulate Your Levels of Happiness

A new study, which used epilepsy patients who had special electrodes implanted in their brains that could monitor hypocretin levels, found that levels of the neurotransmitter soared during positive emotions, anger, social interactions and upon awakening.1

Hypocretin has been previously associated with reward-seeking behaviors, and the researchers suggested it may have a very specific role in human arousal and happiness as well. The study’s lead author, Dr. Jerome Siegel, told the New York Times:2

“This [study] shows that hypocretin is related to a particular kind of arousal … There is an arousal system in the brain whose function is keeping you awake for pleasure, to get rewards. It is related to positive effects, and in its absence you have a deficit in pleasure seeking.”

This explains why people with narcolepsy, who are lacking hypocretin, also commonly suffer from depression. Interestingly, it also suggests there may be other arousal systems in your brain, driven by different brain chemicals, that may be in charge of regulating other specific emotions.

A Warning About Hypocretin-Blocking Sleeping Pills

If an important new biological pathway is discovered you can bet your bottom dollar that the drug companies will not be far behind to manipulate that pathway in some way that will not correct the problem, but merely relieve the symptoms and make them a boatload of money. And that is precisely what has happened.

The U.S. Food and Drug Administration (FDA) has accepted a new drug application for Suvorexant, a new insomnia medication made by Merck.3 This is the same company that brought you Vioxx, which killed 60,000 before being pulled from the market.

The new drug works by targeting hypocretin, temporarily blocking it to help you fall asleep, or, as the New York Times put it, “essentially causing narcolepsy for a night.”4

The concern is that if reduced hypocretin may be responsible for causing depression in narcoleptics, could it also cause depression, or interfere with mood, in healthy people using the hypocretin-blocking drug Suvorexant? So far Merck claims no connection has been found, but there is likely reason for caution:5

“The initial reports are rosy,” Dr. Siegel told the New York Times, “But they come from a drug company with an enormous investment. And there is a long list of drugs acting on the brain whose severe problems were only identified after millions of people were taking them.”

More Proof Lack of Sleep Leads to Weight Gain

Research has only scratched the surface of the far-reaching implications of a disrupted sleep-wake cycle. But in addition to impacting your emotions, it’s known that a lack of sleep causes changes in the hunger and satiety hormones ghrelin and leptin – changes that impact your food intake and ultimately your weight.

The latest research showed the effects of sleeping just five hours a night for five days. The study participants actually burned more energy than those who slept longer, but they had less restraint when it came to mealtime. The sleep-deprived subjects ended up eating more, so that despite their increased energy burning they gained nearly two pounds, on average, during the five-day study.6

Researchers noted:

“Our findings suggest that increased food intake during insufficient sleep is a physiological adaptation to provide energy needed to sustain additional wakefulness; yet when food is easily accessible, intake surpasses that needed … These findings provide evidence that sleep plays a key role in energy metabolism. Importantly, they demonstrate physiological and behavioral mechanisms by which insufficient sleep may contribute to overweight and obesity.”

The good news is that the opposite also held true: when participants started getting more sleep, they subsequently started to eat less and lose weight.

Too Little Sleep Wreaks Havoc on Your Insulin Levels, Leads to Food Cravings

Sleep deprivation tends to lead to food cravings, particularly for sweet and starchy foods. Researchers have suggested that these sugar cravings stem from the fact that your brain is fueled by glucose (blood sugar); therefore, when lack of sleep occurs, and your brain is unable to properly respond to insulin (which drives glucose into brain cells) your brain becomes desperate for carbohydrates to keep going. If you’re chronically sleep deprived, consistently giving in to these sugar cravings will virtually guarantee that you’ll gain weight.

Getting too little sleep also dramatically decreases the sensitivity of your insulin receptors, which will raise your insulin levels. This too is a surefire way to gain weight, as the elevated insulin will seriously impair your body’s ability to burn and digest fat.

According to research published in the Annals of Internal Medicine,7 after four nights of sleep deprivation (sleep time was only 4.5 hours per night), study participants’ insulin sensitivity was 16 percent lower, while their fat cells’ insulin sensitivity was 30 percent lower, and rivaled levels seen in those with diabetes or obesity.

Sleep Deprivation Linked to Psychiatric Disorders

Getting back to the link between sleep, or lack of it, and mood, sleep deprivation is linked to psychiatric disorders such as anxiety and bipolar depression, while getting the right amount of sleep has been linked to positive personality characteristics such as optimism and greater self-esteem, as well as a greater ability to solve difficult problems.8

So there’s no doubt about it: too little sleep can seriously impact your mood and your ability to be happy. If you feel well-rested in the morning, that’s a good sign that your sleep habits are just fine. But if not, you might want to investigate your sleep patterns more closely.

10 Reasons Why You Might Have Trouble Sleeping

There are many factors that can influence your sleep. For my complete recommendations and guidelines that can help you improve your sleep, please see my article 33 Secrets to a Good Night’s Sleep. Following are 10 often-overlooked factors to address if you’re having trouble with your sleep:

    1. Too Much Light in Your Room

Even the tiniest bit of light in the room, including those emitted by electronic devices, can disrupt your pineal gland’s production of melatonin and serotonin, thereby disrupting your sleep cycle.

So close your bedroom door, install black-out drapes, use a sleep mask, get rid of night-lights, and refrain from turning on any light during the night, even when getting up to go to the bathroom. If you have to use a light you can use a red flashlight, as that wavelength of light has a minimal impact on melatonin production.

    1. Exercising Too Close to Bedtime

Exercising for at least 30 minutes per day can improve your sleep. However, don’t exercise too close to bedtime (generally not within the three hours before) or it may keep you awake.

    1. Drinking Alcohol Before Bed

Although alcohol will make you drowsy, the effect is short lived and you will often wake up several hours later, unable to fall back asleep. Alcohol can also keep you from entering the deeper stages of sleep, where your body does most of its healing.

    1. Your Bedroom is Too Warm

Many people keep their homes and particularly their upstairs bedrooms too warm. Studies show that the optimal room temperature for sleep is quite cool, between 60 to 68 degrees F. Keeping your room cooler or hotter can lead to restless sleep. When you sleep, your body’s internal temperature drops to its lowest level, generally about four hours after you fall asleep.

Scientists believe a cooler bedroom may therefore be most conducive to sleep, since it mimics your body’s natural temperature drop.

    1. Caffeine is Keeping You Awake

Caffeine has a half-life of five hours, which means some will still be in your system even 10 hours later, and 12.5% 20 hours later (see the problem?). Plus, in some people caffeine is not metabolized efficiently, leaving you feeling its effects even longer after consumption. So, an afternoon cup of coffee or tea will keep some people from falling asleep at night. Be aware that some over the counter medications contain caffeine as well (for example, diet pills).

    1. You’re Watching the Clock

The more you watch the clock when you wake up in the middle of the night, the more stressed and anxious you will become, and the more you may actually “train” yourself to start awakening at the same time each night. The solution is simple: Remove the clock from your view so you actually have to sit up or change positions to see the clock.

    1. Watching TV to Help You Fall Asleep

The artificial glow from your TV can serve as a stimulus for keeping you awake and, possibly, eating, when you should really be asleep. Further, computer and TV screens (and most light bulbs) emit blue light, to which your eyes are particularly sensitive simply because it’s the type of light most common outdoors during daytime hours. As a result, it can disrupt your melatonin production and further interfere with your sleep.

    1. Worrying in the Middle of the Night

If stress keeps you up at night, try keeping a “worry journal” next to your bedside so you can jot down your thoughts there and clear them from your head. The Emotional Freedom Technique (EFT) can also help balance your body’s bioenergy system and resolve some of the emotional stresses that are contributing to your insomnia at a very deep level. The results are typically long lasting and improvement is remarkably rapid.

    1. Eating Too Close to Bedtime

Although you might struggle with this initially, it is ideal to avoid eating any foods three hours before bed, as this will optimize your blood sugar, insulin and leptin levels and contribute to overall good health.

    1. Smoking

The nicotine in cigarettes is a stimulant, which can keep you awake much as though you just drank a cup of coffee.




park 3

park 2.jpeg

Parkinson’s disease and Mitochondria as the oxygen-consuming power plants of human cells

  • Mitochondrial maintenance is essential for cellular and organismal function.
  • Maintenance includes reactive oxygen species (ROS) regulation, DNA repair, fusion–fission, and mitophagy.
  • Loss of function of these pathways leads to disease.

Mitochondria are the oxygen-consuming power plants of cells. They provide a critical milieu for the synthesis of many essential molecules and allow for highly efficient energy production through oxidative phosphorylation. The use of oxygen is, however, a double-edged sword that on the one hand supplies ATP for cellular survival, and on the other leads to the formation of damaging reactive oxygen species (ROS). Different quality control pathways maintain mitochondria function including mitochondrial DNA (mtDNA) replication and repair, fusion–fission dynamics, free radical scavenging, and mitophagy. Further, failure of these pathways may lead to human disease. We review these pathways and propose a strategy towards a treatment for these often untreatable disorders.

Regarding mitophagy, two landmark papers showed that PINK1 and Parkin, two proteins mutated in familial Parkinson’s disease, are involved in the selective degradation of damaged mitochondria 16 and 100. Loss of these proteins may contribute to the accumulation of damaged mitochondria and death of dopaminergic neurons in the substantia nigra in the mesencephalon.

Further support of a mitochondrial etiology in Parkinson’s disease comes from the early observations that exposure to various mitochondrial toxins leads to Parkinson’s disease in humans and rodents [101]. Interestingly, Parkinsonism is relatively rare in primary mitochondrial diseases indicating that mitochondrial dysfunction does not automatically lead to dopaminergic neuronal death.

Conversely, Parkinson’s disease is not characterized by the severe neurodegeneration that commonly debuts in early adulthood in primary mitochondrial diseases. This may indicate that alternative mitophagy pathways may compensate for defects in PINK1 or Parkin [102] or that mitophagy plays a relatively minor role in overall mitochondrial maintenance. Recent findings of defective mitophagy in neurodegenerative accelerated aging disorders do, however, support a significant role of this pathway in overall mitochondrial maintenance [49].

Mitochondrial genetics

Mitochondria are a dynamic network of organelles constantly adapting their morphology and function to accommodate the needs of the cell. They are composed of an outer membrane, an intermembrane space, a highly folded inner membrane (the cristae), and a matrix space. Due to the prokaryotic origin of this organelle, the inner mitochondria membrane contains a specialized phospholipid, cardiolipin, that is also found in bacteria. More importantly, mitochondria contain their own DNA. The human mitochondrial genome, mtDNA, is a small circular ∼16.6 kilobase molecule that resides inside the matrix space associated with the inner membrane of the mitochondria [1]. mtDNA in humans encodes 13 polypeptides, 22 tRNAs, and two ribosomal genes that are essential for oxidative phosphorylation, the metabolic process by which cells convert energy stored in a range of different substrates to ATP, which is the energetic currency of the organism. All of the remaining mitochondrial proteins, including gene products necessary for mtDNA replication, transcription, and DNA repair, are derived from nuclear genes and are imported into the mitochondria, typically, but not exclusively, via a mitochondrial targeting sequence [2]. In addition to the role of mitochondria in ATP production, this organelle is also central in apoptosis, heme and steroid synthesis, Ca2+ regulation, adaptive thermogenesis, and other processes. Proper mitochondrial function is therefore critical for organismal health.

An understanding of mtDNA inheritance and maintenance patterns is essential for comprehending mitochondrial dysfunction in disease. mtDNA is packaged into protein–DNA structures called nucleoids containing one or more mtDNA genomes within a single nucleoid. Additionally, there are a few to several thousand copies of mtDNA per cell varying with cell type [3]. Cells can simultaneously carry a mixture of normal and mutated mitochondrial genomes, a condition known as heteroplasmy. Mutant mtDNA can be propagated along with normal mtDNA, when there is no selection pressure against the mutant genome, thereby contributing to the high sequence evolution of mtDNA [4]. When a cell divides and the nucleoids are segregated between the two daughter cells, the proportion of mutant to normal mtDNA can shift [5]. This has important ramifications for mitochondrial disease since the relative proportion of mutant mtDNA molecules must reach a certain threshold before a disease phenotype is observed.

Bona fide primary mitochondrial diseases represent a heterogeneous group of disorders most often involving multiple organ systems leading to progressive degeneration and in many cases early death. Since the combined prevalence is estimated to be around 1:5000, a mitochondrial etiology should be considered when encountering any patient, particularly children, with multisystem pathology in tissues such as the central nervous system, heart, skeletal muscles, liver, and in rarer cases kidney [6]. The pathogenic mutation can be located either within the mitochondrial or nuclear genome and, as in the case of mutations in Twinkle or DNA polymerase γ (POLG), can give rise to a great diversity of clinical syndromes (Figure 1).


Life is the interplay between structure and energy, yet the role of energy deficiency in human disease has been poorly explored by modern medicine. Since the mitochondria use oxidative phosphorylation (OXPHOS) to convert dietary calories into usable energy, generating reactive oxygen species (ROS) as a toxic by-product, I hypothesize that mitochondrial dysfunction plays a central role in a wide range of age-related disorders and various forms of cancer. Because mitochondrial DNA (mtDNA) is present in thousands of copies per cell and encodes essential genes for energy production, I propose that the delayed-onset and progressive course of the age-related diseases results from the accumulation of somatic mutations in the mtDNAs of post-mitotic tissues. The tissue-specific manifestations of these diseases may result from the varying energetic roles and needs of the different tissues. The variation in the individual and regional predisposition to degenerative diseases and cancer may result from the interaction of modern dietary caloric intake and ancient mitochondrial genetic polymorphisms. Therefore the mitochondria provide a direct link between our environment and our genes and the mtDNA variants that permitted our forbears to energetically adapt to their ancestral homes are influencing our health today.

Figure 1  Human mitochondrial DNA map showing representative pathogenic and adaptive base substitution mutations. D-loop = control region (CR). Letters around the outside perimeter indicate cognate amino acids of the tRNA genes. Other gene symbols are defined in the text. Arrows followed by continental names and associated letters on the inside of the circle indicate the position of defining polymorphisms of selected region-specific mtDNA lineages. Arrows associated with abbreviations followed by numbers around the outside of the circle indicate representative pathogenic mutations, the number being the nucleotide position of the mutation. Abbreviations: DEAF, deafness; MELAS, mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes; LHON, Leber hereditary optic neuropathy; ADPD, Alzheimer and Parkinson disease; MERRF, myoclonic epilepsy and ragged red fiber disease; NARP, neurogenic muscle weakness, ataxia, retinitis pigmentosum; LDYS, LHON + dystonia; PC, prostate cancer.


As a toxic by-product of OXPHOS, the mitochondria generate most of the endogenous ROS. ROS production is increased when the electron carriers in the initial steps of the ETC harbor excess electrons, i.e., remain reduced, which can result from either inhibition of OXPHOS or from excessive calorie consumption. Electrons residing in the electron carriers; for example, the unpaired electron of ubisemiquinone bound to the CoQ binding sites of complexes I, II, and III; can be donated directly to O2 to generate superoxide anion (O•-2). Superoxide O•-2 is converted to H2O2 by mitochondrial matrix enzyme Mn superoxide dismutase (MnSOD, Sod2) or by the Cu/ZnSOD (Sod1), which is located in both the mitochondrial intermembrane space and the cytosol. Import of Cu/ZnSOD into the mitochondrial intermembrane space occurs via the apoprotein, which is metallated upon entrance into the intermembrane space by the CCS metallochaperone (166, 207). H2O2 is more stable than O•-2 and can diffuse out of the mitochondrion and into the cytosol and the nucleus. H2O2 can be converted to water by mitochondrial and cytosolic glutathione peroxidase (GPx1) or by peroxisomal catalase. However, H2O2, in the presence of reduced transition metals, can be converted to the highly reactive hydroxyl radical (•OH) (Figure 2). Iron-sulfur centers in mitochondrial enzymes are particularly sensitive to ROS inactivation. Hence, the mitochondria are the prime target for cellular oxidative damage (241, 242).


The mitochondria are also the major regulators of apoptosis, accomplished via the mitochondrial permeability transition pore (mtPTP). The mtPTP is thought to be composed of the inner membrane ANT, the outer membrane voltage-dependent anion channel (VDAC) or porin, Bax, Bcl2, and cyclophilin D. The outer membrane channel is thought to be VDAC, but the identity of the inner membrane channel is unclear since elimination of the ANTs does not block the channel (98). The ANT performs a key regulatory role for the mtPTP (98). When the mtPTP opens, ΔP collapses and ions equilibrate between the matrix and cytosol, causing the mitochondria to swell. Ultimately, this results in the release of the contents of the mitochondrial intermembrane space into the cytosol. The released proteins include a number of cell death-promoting factors including cytochrome c, AIF, latent forms of caspases (possibly procaspases-2, 3, and 9), SMAD/Diablo, endonuclease G, and the Omi/HtrA2 serine protease 24. On release, cytochrome c activates the cytosolic Apaf-1, which activates the procaspase-9. Caspase 9 then initiates a proteolytic cascade that destroys the proteins of the cytoplasm. Endonuclease G and AIF are transported to the nucleus, where they degrade the chromatin. The mtPTP can be stimulated to open by the mitochondrial uptake of excessive Ca2+, by increased oxidative stress, or by deceased mitochondrial ΔP, ADP, and ATP. Thus, disease states that inhibit OXPHOS and increase ROS production increase the propensity for mtPTP activation and cell death by apoptosis (Figure 2) (241, 242).

Clinical symptoms appear when the number of cells in a tissue declines below the minimum necessary to maintain function. The time when this clinical threshold is reached is related to the rate at which mitochondrial and mtDNA damage accumulates within the cells, leading to activation of the mtPTP and cell death, and to the number of cells present in the tissue at birth in excess of the minimum required for normal tissue function. Given that the primary factor determining cell metabolism and tissue structure is reproductive success, it follows that each tissue must have sufficient extra cells at birth to make it likely that that tissue will remain functional until the end of the human reproductive period, or about 50 years. If the mitochondrial ROS production rate increases, the rate of cell loss will also increase, resulting in early tissue failure and age-related disease. However, if mitochondrial ROS production is reduced, then the tissue cells will last longer and age-related symptoms will be deferred (236, 238, 241) (Figure 3).

Type II diabetes thus involves mutations in energy metabolism genes including the mtDNA and glucokinase; mutations in the transcriptional control elements PPARγ, PGC-1, HNF-1α, HNF-4α, and IPF-1; and alterations in insulin signaling. These seemingly disparate observations can be unified through the energetic interplay between the various organs of the body.

Notorious variability in the presentation of mitochondrial disease in the infant and young child complicates its clinical diagnosis. Mitochondrial disease is not a single entity but, rather, a heterogeneous group of disorders characterized by impaired energy production due to genetically based oxidative phosphorylation dysfunction. Together, these disorders constitute the most common neurometabolic disease of childhood with an estimated minimal risk of developing mitochondrial disease of 1 in 5000. Diagnostic difficulty results from not only the variable and often nonspecific presentation of these disorders but also from the absence of a reliable biomarker specific for the screening or diagnosis of mitochondrial disease. A simplified and standardized approach to facilitate the clinical recognition of mitochondrial disease by primary physicians is needed. With this article we aimed to improve the clinical recognition of mitochondrial disease by primary care providers and empower the generalist to initiate appropriate baseline diagnostic testing before determining the need for specialist referral. This is particularly important in light of the international shortage of metabolism specialists to comprehensively evaluate this large and complex disease population. It is hoped that greater familiarity among primary care physicians with the protean manifestations of mitochondrial disease will facilitate the proper diagnosis and management of this growing cohort of pediatric patients who present across all specialties.



Increased oxidative stress due to coenzyme Q10 (CoQ10) deficiency leads to an adaptive increase in autophagy [112]. Additionally, it has recently been shown that a defect in mitochondrial protein maintenance can augment autophagy [113]. It follows that a decrease in ROS production will lead to a decrease in the mitochondrial maintenance pathways. This tight regulation of mitochondrial maintenance through ROS is a possible explanation for the disappointing results antioxidants have shown in some human trials.

Food sources: COQ10

CoQ10 is naturally found in high levels in organ meats such as liver, kidney, and heart, as well as in beef, sardines, and mackerel. Vegetarians or vegans who are used to eating these foods should find a suitable alternative. Luckily, vegetable sources of CoQ10 include spinach, broccoli, and cauliflower.


Includes lean meats, poultry, seafood, beans and peas, eggs, and nuts and seeds. Pork, beef, turkey, chicken, fish, shellfish, mushrooms, whole grains and eggs contain high amounts of selenium. Some beans and nuts, especially Brazil nuts, contain selenium.

A link to your signup form:

Subscribe to our mailing list

Powered by Robly