Probiotic and Gut Brain connection

Gut and brain connection is not new to us, but to what extent and how it affects all aspects of our wellbeing or illness that we succumb to is being explored constantly in science.

Gut brain connection is not only the connection of Vagus nerve to the brain, but the bacteria that live in gut, and how its various metabolic products affect brain is another powerful connection.

We note that depression is related to inflammation and genesis of inflammation, for the most part is in gut. The article mentions that we are not at this stage where we can treat depression with probiotics alone. I agree.
That is even more the reason to care for our microbiome in our GI tract. Our lifestyle choices, the food we eat, stress we carry, sedentary or active life we live, relations and community we keep, and allow are body and mind to rest does affect our microbiome. That in turn affects genesis of inflammation through our gut.
This article in Men’s health magazine caught my eyes.

Probiotic and gut brain connection-

Diseases Rooted in Gut Microbiome and what to do about it:

The microorganisms in an environment (including the body or a part of the body) are called microbiome.

Scientists at the Weizmann Institute of Science redid the estimate and found that there are about 39 trillion bacterial cells in the body. They play a profoundly important role in human health and disease, from helping us absorb nutrients, to synthesizing vitamins and breaking down cellulose. We couldn’t survive without this microbial zoo inside us.

Shortly after birth, we are colonized with over 1000 species of gut bacteria. Influences such as vaginal delivery vs Cesarean section, breast-feeding vs bottle feeding, antibiotic use, industrialized processed food, heavy metal toxicity, stress levels, chronic illness and poor dietary choices, glyphosate in non-organic foods all have a profound impact on which bugs are selectively destroyed  leading to further imbalance and disease.

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Diseases Rooted in Gut Microbiome and what to do about it:

Early Alzheimer’s, mild or subjective neurocognitive decline, “brain fog” Is it permanent? NO. Thanks to Functional Medicine / Dr. Bredesen’s approach

According to Alzheimer’s association 2017 fact and figures-
“-Alzheimer’s is the 6th leading cause of death in USA
-35% of caregivers for people with Alzheimer’s or other dementia report that their health has gotten worse due to care responsibilities compared to 19% of caregivers for older people without dementia
-1 in 3 seniors dies with Alzheimer or another dementia
-Since 2000, deaths from heart disease have decreased by 14%,while deaths from Alzheimer’s disease have increased by 89%.”

When older patients and their families report symptoms of “memory loss,” experienced clinicians know that these concerns refer to a range of cognitive abilities or to general cognitive decline, and not just memory. .

Cognitive decline is a major concern of the aging population, and Alzheimer’s disease is the major cause of age-related cognitive decline. Unlike several other chronic illnesses, Alzheimer’s disease prevalence is on the rise. Approximately 5.5 million suffer from this disease in America and 46 million globally.

Neurocognitive disorders, , have tremendous consequences for individuals, their families, the healthcare system, the economy. In the United States, Alzheimer’s disease (AD) is a leading cause of death, hospital admissions, skilled nursing facility admissions, and home health care (1). Family caregivers also experience increased emotional stress, depression, and health problems (2).

Some of the risk factors for neurocognitive decline

AGE –Increasing age is not only the strongest risk factor for dementia, but also the only risk factor consistently identified after the eighth decade of life. There are other causes for mild cognitive decline in younger populations.

GENES –While several genes have been identified as increasing susceptibility for Alzheimer’s disease, the best-established is the Apolipoprotein E (APOE) polymorphism on Chromosome 19. The APOE*4 allele, associated with higher risks of hypercholesterolemia and heart disease, is also associated with dementia due to Alzheimer’s and Parkinson’s diseases, Dementia with Lewy Bodies, vascular dementia, and frontotemporal dementia in men.

MEDICAL –The medical risk factors are, cardiovascular disease, hypertension, high cholesterol, high body mass index, diabetes etc.

INFLAMATION/INFECTIONS –Inflammation and inflammatory markers like interleukins, cytokines, CRP, has been reported in Alzheimer’s and vascular dementia. Inflammation because of any infection, heavy metal toxicity, high blood sugar, increased stress, mold ,Lyme dieses etc. (3) (4).

SLEEP–Sleep apnea is associated with hypertension, heart disease and increased risk of stroke, white matter changes in brain with increased risk of dementia (5).

DEPRESSION –Depression has a complex and likely bidirectional association with dementia. Recurrent major depression in earlier adulthood appears to increase risk of dementia in later life (6).

ANXIETY–Late-life anxiety is associated with cognitive impairment and decline Late-life anxiety and cognitive impairment: a review.

PTSD–Posttraumatic stress disorder has been reported to increase the risk of dementia and mild cognitive impairment. Posttraumatic stress disorder and risk of dementia among US veterans.

SENSE OF PURPOSE –Lifelong traits of harm avoidance and lesser sense of purpose have been reported as harbingers of AD. Harm avoidance and risk of Alzheimer’s disease.

HEAD TRAUMA –Head trauma is associated with increased risk of dementia, and the severity of injury appears to heighten this risk. Neurocognitive disorders can occur immediately after a traumatic brain injury or after the recovery of consciousness at any age. However, chronic traumatic encephalopathy is diagnosed years after repeated concussive or sub concussive blows to the head, with a clinical presentation similar to AD (Alzheimer Disease) or frontotemporal lobar degeneration. Mild traumatic brain injury.

TOXINS –Many environmental and occupational exposures have been associated with neurodegenerative disease. Neurodegenerative diseases: an overview of environmental risk factors. Smoking has been associated with an elevated risk of dementia. Smoking as a risk factor for dementia and cognitive decline. Heavy consumption of alcohol increases odds of developing dementia. Parkinson’s disease risk is associated with exposure to pesticides, for which a molecular mechanism has been established. Molecular mechanisms of pesticide-induced neurotoxicity.

Protective factors

Protective factors are those which reduce incidence rate or reduced odds of dementia. Cognitive reserve refers to its functional capacity, specifically the ability to utilize alternative neural networks and compensatory strategies. What is cognitive reserve?

EDUCATION–Where educational opportunities are universal, higher education may reflect innate reserve; the process of education may also promote the development of reserve through mechanisms such as increased dendritic branching. Regardless of mechanism, higher education is associated with lower prevalence of dementia. Education and dementia.

LANGUAGE–Bilingualism has been associated with delayed onset of dementia, independent of education, and may specifically protect against declines in attention and executive functioning. Delaying the onset of Alzheimer disease. Bilingualism delays age at onset of dementia.

COGNITIVE ACTIVITY–Cognitive activity: Lifelong occupations that do not require higher education or skilled vocational training appear to be associated with a higher risk of dementia. Education and occupation as risk factors for dementia Education, occupation, and dementia. Cognitively stimulating activities appear to have both protective and enhancing effects on cognition.

LEISURE ACTIVITIES–Several popularly usual activities such as reading, playing board games, playing musical instruments, and dancing are associated with a reduced risk of dementia. Leisure activities and the risk of dementia in the elderly.

LIFE STYLE FECTORS–As mentioned above Mediterranean diet, high physical activity, stress reduction, good nutrition, restful sleep, community involvement, and less exposure to toxins are protective factors. It is difficult to cover all protective methods here.

Simple “Brain fog” is a state of temporary cognitive impairment. Early Alzheimer’s disease and mild cognitive decline does not always have to progress to dementia. Keep in mind above risk and protective factors and start correcting them.

As Dr. Bredesen says “Neurodegenerative disease therapeutics has been, arguably, the field of greatest failure of biomedical therapeutics development. Patients with acute illnesses such as infectious diseases, or with other chronic illnesses, such as cardiovascular disease, osteoporosis, human immunodeficiency virus infection, and even cancer, have access to more effective therapeutic options than do patients with AD or other neurodegenerative diseases such as Lewy body dementia, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis. In the case of Alzheimer’s disease, there is not a single therapeutic that exerts anything beyond a marginal, unsustained symptomatic effect, with little or no effect on disease progression. Furthermore, in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one.”

Dr. Bredesen’s approach utilizes functional medicine approach. 21st-century medicine is completely different. Larger data sets are used to identify network changes that characterize chronic illnesses, revealing the “why” for each person. Addressing the cause of each condition in a comprehensive and personalized, programmatic way leads to improved outcomes.

Such an approach was used to bring about the first reversal of cognitive decline in patients with early Alzheimer’s disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), published in 2014 (Bredesen, Aging 2014).



Mast Cell Activation Syndrome (MCAS):When Histamine causes problem

Mast cells are present in most tissues throughout the human body, especially connective tissue, skin, intestinal lining cardiovascular system, nervous system, and reproductive organs. They are part of the allergic response designed to protect us from threat and injury. When the body is exposed to a perceived threat, the mast cells secrete chemical mediators, such as histamine, interleukins, prostaglandins, cytokines, chemokine and various other chemicals stored in the cytoplasm of the cell. These chemical messengers produce both local and systemic effects, such as increased permeability of blood vessels (inflammation and swelling), contraction of smooth muscle (stomach cramps and heart palpitations), and increase mucous production (congestion, sneezing, etc). Historically, we thought of mast cells only in relation to an allergic or anaphylactic response. We now know they play a profound role in immune activation, development of autoimmunity and many other disorders, such as POTS (postural orthostatic tachycardia syndrome). Sadly we are seeing a large increase in patients presenting with mast cell disorders and MCAS. I believe it is in part due to the onslaught of more pervasive environmental toxins, molds and chemicals.

Without mast cells, we would not be able to heal from a wound. They protect us from injury and help the body to heal. Unfortunately, overactive mast cells can cause a variety of serious symptoms.

Symptoms of overactive mast cells may include:
  •  skin rashes/hives
  • swelling/edema
  •  flushing
  •  itching
  •  abdominal pain
  • nausea/vomiting
  • diarrhea
  • wheezing
  • shortness of breath
  • heart palpitations
  • anxiety, difficulty concentrating
  • headaches
  • brain fog
  • low blood pressure
  • fatigue

Mast cell activation syndrome (MCAS) is a condition symptoms involving the skin, gastrointestinal, cardiovascular, respiratory, and neurologic systems. It can be classified into

  • primary (clonal proliferation or mastocytosis),
  • secondary (due to a specific stimulus), and
  • idiopathic (no identifiable cause).

Proposed criteria for the diagnosis of MCAS included episodic symptoms consistent with mast cell mediator release affecting two or more organ systems with hives, swelling, flushing, nausea, vomiting, diarrhea, abdominal pain, low blood pressure, fainting, heart palpitations, wheezing, red eyes, itching, and/or nasal congestion. For a diagram of all of the varied symptoms histamine can cause.

Triggers may be medications, foods, supplements, hormones, opioids, stressors (physical or emotional), cold temperature, heat, pressure, noxious odors, chemicals, insect bites, trauma or environmental toxins.
We commonly see mast cell activation syndromes associated with CIRS (chronic inflammatory response syndrome) in response to biotoxins, such as mold, inflammagens, and lyme-related toxins.

Low MSH and Mast Cell Disorders?

As mentioned above, we frequently see histamine intolerance and MCAS in patients with mold-related CIRS (chronic inflammatory response syndrome). It is interesting to note that a common finding in CIRS is low MSH. According to this study in the Journal of Investigative Dermatology, alpha-MSH plays an immunomodulatory role during inflammatory and allergic reactions of the skin. In addition, there is evidence that MSH induces mast-cell apoptosis (cell death).

Definition of Mast Cell Activation Syndrome (MCAS)

1. Typical clinical symptoms as listed above
2. Increase in serum tryptase level or an increase in other mast cell derived mediators, such as histamine or prostaglandins (PGD2), or their urinary metabolites,
3. Response of symptoms to treatment

Mast Cell Activation

Mast cells can be activated by both direct and indirect mechanisms as a result of exposure of the host to pathogens.

Diseases Associated with Mast Cell Activation Syndrome (MCAS)

• Allergies and Asthma
• Autism
• Autoimmune diseases (Hashimoto’s thyroiditis, systemic lupus, multiple sclerosis, bullous pemphigoid, rheumatoid arthritis and others.Eczema
• Celiac Disease
• Chronic Fatigue Syndrome
• CIRS (chronic inflammatory response syndrome)
• Eosinophilic Esophagitis
• Fibromyalgia
• Food Allergy and Intolerances
• Gastroesophageal reflux (GERD)
• Infertility (mast cells in endometrium may contribute to endometriosis)
• Interstitial Cystitis
• Irritable Bowel Syndrome (IBS)
• Migraine Headaches
• Mood disorders – anxiety, depression, and insomnia
• Multiple Chemical Sensitivities
• POTS (postural orthostatic hypotension)

Cytokines and chemicals production with mast cell activation

Mast cells are known to be the primary responders in allergic reactions, orchestrating strong responses to minute amounts of allergens. Several recent observations indicate that they may also have a key role in coordinating the early phases of autoimmune diseases, particularly those involving auto-antibodies.

Lab Tests for Mast Cell Activation Syndrome (MCAS)

• Lab tests specific to mast cell activation for suspected MCAS may include:
• Serum tryptase (most famous mast cell mediator)
• Serum chromogranin A
• Plasma histamine
• Plasma PGD2 (chilled)
• Plasma heparin (chilled)
• Urine for PGD2 (chilled)
• PGF2a
• N-methylhistamine
• Tryptase is the most famous mast cell mediator. Serum tryptase value is usually normal in MCAS patients, but sometimes it is elevated. Tryptase values that show an increase of 20% + 2 ng/ml above the baseline level are considered diagnostic for MCAS.
• Chromogranin A is a heat-stable mast cell mediator. High levels can suggest MCAS, but other sources must first be ruled out, such as heart failure, renal insufficiency, neuroendocrine tumors and proton pump inhibitor (PPI) use.
• Heparin is a very sensitive and specific marker of mast cell activation. However, due to its quick metabolism in the body, it is very difficult to measure reliably.
• N-methylhistamine is usually measured in a 24 hour urine test to account for the variability in release over the course of the day.
• Prostaglandin D2 is produced by several other cell types, but mast cell release is responsible for the dominant amount found in the body. PGD2 is less stable than histamine and metabolized completely in 30 minutes.
• Other less specific mast cell mediators that are sometimes abnormal in MCAS patients include Factor VIII, plasma free norepinephrine, tumor necrosis factor alpha, and interleukin-6.

Treatments to reduce MCAS symptoms and lower histamine

#1 histamine 1 and 2 blockers
#2 leukotriene inhibitors like Singulair
#3 mast cell stabilizer like Chromelin
#4 Natural mast cell stabilizer like vitamin C, quercetine certain probiotics
#5 DAO enzyme with meals like histDAO
#6 reduce consumption of high histamine food
• Avoid alcoholic beverages
• Avoid raw and cured sausage products such as salami.
• Avoid processed or smoked fish products. Use freshly caught seafood instead.
• Avoid pickles
• Avoid citrus fruits.
• Avoid chocolate
• Avoid nuts
• Avoid products made with yeast and yeast extracts
• Avoid soy sauce and fermented soy products
• Avoid black tea and instant coffee
• Avoid aged cheese
• Avoid spinach in large quantities
• Avoid tomatoes, ketchup and tomato sauces
• Avoid artificial food colorings & preservatives
• Avoid certain spices: cinnamon, chili powder, cloves, anise, nutmeg, curry powder, cayenne pepper

As mast cell activation condition, can present in many ways. Important thing is for your physician needs to recognize the presence of this condition. It is manageable and symptoms can be controlled. I would advise you to find a physician who is willing to work with you in this condition.

Lessening the Power of Negative Emotion

The mind, body, and spirit are intimately connected with our physiology (body’s working). Our mental, spiritual and emotional well-being affects our neuro-hormonal system immensely. I have many times advised my patients to incorporate “medical journaling” for health and vitality..
I came across this writing from “The Dalai Lama”</Font color> and would like to share with you.

I profoundly believe that real spiritual change comes about not by merely praying or wishing that all negative aspects of our minds disappear and all positive aspects blossom. It is only by our concerted effort, an effort based on an understanding of how the mind and its various emotional and psychological states interact, that we bring about true spiritual progress. If we wish to lessen the power of negative emotions, we must search for the causes that give rise to them. We must work at removing or uprooting those causes. At the same time, we must enhance the mental forces that counter them: what we might call their antidotes. This is how a meditator must gradually bring about the mental transformation he or she seeks.

How do we undertake this? First we identify our particular virtue’s opposing factors. The opposing factor of humility would be pride or vanity. The opposing factor of generosity would be stinginess. After identifying these factors, we must endeavor to weaken and undermine them. While we are focused on these opposing factors, we must also be fanning the flames of the virtuous quality we hope to internalize. When we feel most stingy, we must make an extra effort to be generous. When we feel impatient or judgmental, we must do our utmost to be patient.

When we recognize how our thoughts have particular effects upon our psychological states, we can prepare ourselves for them. We will then know that when one state of mind arises, we must counter it in a particular way; and if another occurs, we must act appropriately. When we see our mind drifting toward angry thoughts of someone we dislike, we must catch ourselves; we must change our mind by changing the subject. It is difficult to hold back from anger when provoked unless we have trained our mind to first recollect the unpleasant effects such thoughts will cause us. It is therefore essential that we begin our training in patience calmly, not while experiencing anger. We must recall in detail how, when angry, we lose our peace of mind, how we are unable to concentrate on our work, and how unpleasant we become to those around us. It is by thinking long and hard in this manner that we eventually become able to refrain from anger.

One renowned Tibetan hermit limited his practice to watching his mind. He drew a black mark on the wall of his room whenever he had an unvirtuous thought. Initially his walls were all black; however, as he became more mindful, his thoughts became more virtuous and white marks began to replace the black ones. We must apply similar mindfulness in our daily lives.

You can also draw upon one or more during the activity if your attention is flagging. They are listed in an order that makes sense to me, but you can vary the sequence.

1. Set the intention to sustain your attention, to be mindful. You can do this both top-down, by giving yourself a gentle instruction to be attentive, and bottom-up, by opening to the sense in your body of what mindfulness feels like.

2. Relax. For example, take several exhalations that are twice as long as your inhalations. This stimulates the calming, centering parasympathetic nervous system and settles down the fight-or-flight stress-response sympathetic nervous system that jiggles the spotlight of attention this way and that, looking for carrots and sticks.

3· Without straining at it, think of things that help you feel cared about-that you matter to someone, belong in a relationship or group, are seen and appreciated, or are even cherished and loved. It’s OK if the relationship isn’t perfect, or that you bring to mind
people from the past, or pets, or spiritual beings. You could also get a sense of your own goodwill for others, your own compassion, kindness, and love. Warming up the heart in this way helps you feel protected, and it brings a rewarding juiciness to the moment-which support #4 and #5 below.

4· Think of things that help you feel safer, and thus more able to rest attention on your activities, rather than vigilantly scanning. Notice that you are likely in a relatively safe setting, with resources inside you to cope with whatever life brings. Let go of any unreasonable anxiety, any unnecessary guarding or bracing.

5· Gently encourage some positive feelings, even mild or subtle ones. For example, think of something you feel glad about or grateful for; go-to’s for me include my kids, Yosemite, and just being alive. Open as you can to an underlying sense of well-being that may nonetheless contain some struggles or pain. The sense of pleasure or reward in positive emotions increases the neurotransmitter, dopamine, which closes a kind of gate in the neural substrates of working memory, thus keeping out any ”barbarians,” any invasive distractions.

6. Get a sense of the body as a whole, its many sensations appearing together each moment in the boundless space of awareness. This sense of things as a unified gestalt, perceived within a large and panoramic perspective, activates networks on the sides of the brain (especially the right-for right-handed people) that support sustained mindfulness. And it de-activates the networks along the midline of the brain that we use when we’re lost in thought.

7. Stay with whatever positive experiences you’re having or lessons you’re learning, for 10-20-30 seconds in a row. Since “neurons that fire together, wire together,” this savoring and registering helps weave the fruits of your attentive efforts into the fabric of your brain and yourself.

Can a Poo Transplant Help You Lose Weight?

We know that fecal (stool, Poo) transplant is recently talked about in medical treatment. Here are some interesting implications that are being investigated. I thought this could be interesting read. Here is an article written by Dr Gerry Mullin.

Your gut flora is a highly diverse ecosystem whose composition is as unique as your fingerprint. The more diverse it is, the healthier you are. Your gut ecosystem is also delicately balanced between many friendly symbiotes and a limited number of potentially harmful pathogens that are prevented from gaining a foothold and triggering an aggressive immune response.

There are times, however, when your gut’s garden gets out of balance, resulting in an overabundance of pathogens and/or a deficiency of beneficial bacteria. This is called dysbiosis — a state of microbial imbalance related to your gut ecosystem, your skin, your inner ear, or any of the other communities of microbes in your body. The scientific literature is quite robust in connecting dysbiosis of human ecosystems to adverse health outcomes. Science is linking dysbiosis to obesity and diabetes (aka diabesity), and there are abundant data in mice showing how lean mice can become fat through stool transplants from fat mice.

Scientists at the Center for Genome Science and Systems Biology at Washington University in St. Louis asked themselves a simple question: Does gut flora influence weight gain? To find the answer, they designed an interesting experiment. They took two groups of mice whose digestive tracts had been sterilized. In the first group, they colonized the mice’s intestines with flora from an obese cage mate. In the second group, they colonized the intestines with flora from a lean mouse. They then fed these two groups of mice the same diet for 2 weeks. At the end of 2 weeks, the mice that were inoculated with the obese microbiome had gained more weight than the mice exposed to the lean mouse’s gut microbiome, despite equivalent food intake and activity. (Turnbaugh PJ, Backhed F, Fulton L, Gordon JI. Diet-induced obesity is linked to marked but reversible alterations in the mouse distal gut microbiome. Cell Host . 2008;3(4):213-23.)

This experiment shows that there are specific types of gut flora that cause you to gain fat—and other types that lead to weight loss. The type that’s dominant will dictate how much fat you accumulate. Many scientists term this “infect obesity”. This finding has led to an explosion of research which clearly links a dysbiotic gut flora to aberrant metabolic consequences such as diabesity.
A very interesting research finding was published in the journal Science. A study led by Dr. Jeffrey Gordon from Washington University showed that mice when fed microbes from obese people tended to gain weight but microbes from lean people protected mice from excessive weight gain-even when fed a high-fat low fiber diet that we call “The Standard American Diet” or SAD Diet”. In another “housing” experiment, lean mice were found to transfect obese mice with their healthy microbiota — “converting” the obese microbiome to a lean one which led to weight loss. But here is the catch. In order for this to happen the obese mice had to be eating a high fiber low saturated fat diet to help support the colonization of the healthy microbes form the lean mice. These findings were published in Science September 6, 2013;vol 341:6150.

There have been interesting preliminary human trials using fecal bacteriotherapy (FBT) — the transfer of intestinal flora from one individual to another to establish a healthy guts microbiome in the recipient. In other words, these “poo transplants” take the feces of someone with a healthy microbiome and introduce it into someone who lacks one.
Most of the FBT studies so far have been conducted to determine whether this intervention would be an effective way to fight recurrent Clostridium difficile infection (CDI) which is usually seen after the use of antibiotics. Once successfully treated with antibiotics, CDI has a high recurrence (>25%) since these antimicrobials generate dysbiosis that is characterized by a reduced diversity of the microbiota which favors the growth of pathogenic species. CDI is a highly contagious diarrheal illness that is increasingly common in hospitals and can be lethal. Of the more than 400 cases of recurrent CDI that have been treated with FBT so far, the cure rate is over 90 percent for those with a potentially life-threatening infection that that is resistant to all other aggressive medical therapy. This is a powerful model for showing how dangerous dysbiosis can be and how rebalancing the gut ecosystem by infusing a healthy mix of gut microbes can produce dramatic results.

The million-dollar question: Are poo transplants an effective intervention for weight problems? Though they’re not a cure for obesity, they appear to be capable of shifting one toward a lean metabolism. In 2010, a double-blind randomized controlled trial on the use of FBT for diabetes and obesity was conducted in 18 male subjects. Half received fecal material from lean male donors; half were implanted with their own feces. After 6 weeks, those who received fecal transplants from lean donors saw a marked reduction in fasting triglyceride levels and significant improvement in insulin sensitivity. (Vrieze A, Holleman F, Zoetendal EG, de Vos WM, Hoekstra JB, Nieuwdorp M. The environment within: how gut microbiota may influence metabolism and body composition. Diabetologia. 2010;53(4):606-13. El-Matary W, Simpson R, Ricketts-Burns N.). This is a small test group, but the results were replicated in a similar follow-up study by the same researchers, so the science is promising.

Does that mean you’ll be able to walk into your doctor’s office in the near future and ask for a poo transplant to improve diabetes or lose weight? Not likely. The safety of fecal transplantation has never been formally investigated long term, and clinicians have expressed concerns about FBT “opening up a can of worms” after 4 of 77 patients developed a de novo autoimmune disease after FBT. (Fecal microbiota transplantation: are we opening a can of worms? Gastroenterology. 2012;143(2):e19; author reply e-20.) Furthermore, the FDA limited the practice of FBT to those with CDI-associated diarrhea that failed conventional medical therapy provided donors are properly screened and patients are informed that fecal transplants are still experimental.

This is an exciting area of research. The Johns Hopkins University School of Medicine and its dean, Dr. Paul Rothman, have formed a microbiome interest group led by Drs. Cynthia Sears and Glenn Treisman to set priorities and to collaborate and pool resources. I’m ( Dr Mullin) fortunate to be working with this distinguished team of investigators. Dr. Linda A. Lee, leads the Johns Hopkins FBT program. Dr. Lee is a pioneer and leader in the field of integrative gastroenterology and director of The Johns Hopkins Integrative Medicine & Digestive Center and is Clinical Director for the Division of Gastroenterology at Johns Hopkins Hospital.

Research on FBT may pave the way for more targeted, safer interventions for obesity, irritable bowel syndrome, inflammatory bowel problems, metabolic syndrome, and more.

Night time binges and weight—my thoughts

Do you find yourself binging at night? You are not alone! . Millions other suffer from this devastating problem and that can lead to depression, fibromyalgia, obesity, fatigue, rashes, migraines, food allergies, high cholesterol, digestive problems etc
If you eat late at night just before bed, you will gain weight. Your body will store the extra calories as fat instead of processing and burning them. How does this happen? Why even after a big meal, we crave more food, more sugar, dessert, chips, and other unhealthy foods?
It is not psychological or emotional problem alone. (For some, night eating is triggered by emotions, stress of any sort). One of the underlying causes is an imbalance of the hormones that regulate appetite. These appetite hormones are insulin, Ghrelin, leptin, peptide YY and cortisol (the stress hormone.).

Insulin</FONT COLOR>

Insulin is a very important hormone that our body produces to process carbohydrate and sugar in diet. After meal when blood sugar goes up, insulin goes up and helps glucose up take in the cells, thus normalizing blood sugar. Insulin is appetite suppressor in our brain.

Ghrelin</FONT COLOR>

Ghrelin is a peptide produced by cells in the gastrointestinal tract (1, 2.) It regulates hunger, increase gastric acid secretion and gut motility. When stomach is empty it is secreted making us feel hungry, when stomach is full and stretched its secretion stops giving us feeling of full stomach.


It is a peptide that in human is secreted by cells in small intestine and colon in response to eating. In the blood and gut, PYY acts to reduce appetite, inhibit gastric motility which increases the efficiency of digestion, increases water and electrolyte absorption in the colon.


Leptin is a hormone made by fat cells which regulates the amount of fat stored in the body (3). When there is set amount of fat in the cell, leptin is secreted, which works on hypothalamus to inhibit hunger. This is a very complex process involving multitude of other hormones (4, 5, 6)

Cortisol</FONT COLOR>

When we are stressed, cortisol level goes up, which makes us hungry, blood sugar and insulin level rises. This sets the stage for insulin resistance and prediabetes.
So it is important to pay some more attention to balancing our hormone and help stop cravings and nighttime binges.


*Eat breakfast–when you eat late at night, you will not be hungry in the morning for breakfast. We need to break this cycle, so start with good protein breakfast. You can have whole free range pasture fed egg in any form you like for portion of protein (which helps balance blood sugar), or have protein shake, as I do, with hemp seed, pumpkin seeds, walnuts, almond butter, frozen blueberries, strawberries, apple skins, with almond milk, with 10-15 gm of Rice, pea or whey protein. Put them all in a blender and get your morning shake.

*Avoid drinking empty calories in form of sodas, juice, sports drinks, iced tea etc. This spikes the insulin and blood sugar levels and finally results in cravings.

*Eat regularly, have breakfast, lunch and dinner and if you need small healthy snack in between, but eat at regular time.

*It is important to have protein and good quality fat at every meal. Seeds, avocado, olive oil, walnuts, are good sources of fat. Quality protein like free range chicken, wild fish, grass fed meat, plus lots of multicolor organic vegetables, fruits, legumes, beans.

*It is important to pause during the daytime, to reduce stress. Choose a method like yoga, abdominal breathing, meditation, or gentle exercise or a book you like to read, or listen to soothing music. Any of these methods that bring you back to Center, reduce stress, balance brain chemistry, and brings hormone in balance.

*It is important to have good sleep habit and have a good night’s sleep. When we deprive ourselves of sleep, Ghrelin goes up making us feel hungry and, Peptide YY, the hormones which make us feel full, goes down.

*It is very important to find food sensitivities, people do not realize this, but we often crave the things we are allergic to or sensitive to. Gluten and dairy are the biggest triggers for food sensitivity and leaky gut.

*If you are deficient in vitamin D, it needs to be checked as vitamin D helps regulate hormones.

*While following these suggestions, do not forget the Center of your being is your mental, emotional, and spiritual make up. Do not forget to nurture your own self.
Bringing hormones in balance, by attention to our life style choices, we can curb our cravings. We can bring improvement in chronic conditions like depression, diabetes, obesity, fatigue, high cholesterol, muscle aches and pains and much more.

Let us all be well.

Is There Anything Like Non-Celiac Gluten Sensitivity

Systemic Immune Response Discovered</FONT COLOR>

Many of my patients come with completely normal evaluation but have no answer for their symptoms. I came across some information that I thought would be interesting.

Many patients report symptoms when consuming gluten, but are negative for serum markers of celiac disease. This so-called non-celiac gluten sensitivity has been maligned in mainstream medicine for years, but new studies point to the potential mechanisms for this effect.

A recent study investigated immune responses in 80 individuals with non-celiac wheat sensitivity who reported gastrointestinal symptoms after consuming wheat products. The control groups consisted of healthy controls as well as individuals with diagnosed celiac disease. All participants adhered to a wheat-, barley-, and rye-free diet for 6 months. Reintroduction of wheat products led to relapse and measurable increase in symptoms.

The key finding was in the serum samples. The researchers discovered changes in biomarkers for the non-celiac wheat-sensitive group. When these participants consumed a diet including wheat, IgG, IgA, and IgM antibodies were significantly higher than in the healthy control group. On the other hand, IgA reactivity was lower than in the celiac group. Serum levels of markers for systemic immune response (LBP- lipopolysaccharide binding protein-and sCD14 measurements) were significantly higher in the non-celiac wheat-sensitive group than in either the healthy or celiac groups. This systemic immune activation correlated with intestinal epithelial damage (measured with FABP2) in both the non-celiac wheat-sensitive group and the celiac group.1

The study also tested serum samples after wheat, barley, and rye were eliminated from the diet. After 6 months of the restricted diet, all participants had significantly improved biomarkers. IgG, IgA, and IgM anti-gliadin antibodies were reduced, as well as LBP, sCD15, EndoCAb IgM, and anti-flagellin IgG and IgM antibodies. Patients’ self-reported symptoms also declined significantly. The systemic immune activation went down as well, paralleling the decrease in reported symptoms.

Importantly, non-celiac wheat-sensitive patients did not show the typical celiac biomarker profile. They did not have elevated antibody responses to TG2 or deamidated gliadin sequences. Duodenal biopsies did not reveal villous atrophy or mucosal abnormalities. However, non-celiac wheat-sensitive participants did have measurable intestinal barrier defects and systemic immune activation.

Another recent study provided further evidence that reintroducing gluten can lead to symptoms in subsets of patients without celiac disease. A double-blind, placebo-controlled trial with 18 patients tested gluten or placebo added to participants’ regular, gluten-free diet. All participants had lymphocytic enteritis without celiac serum markers, but were positive for HLA-DQ2/8, a significant risk factor for celiac disease. More than 90% of the group who received the gluten challenge relapsed and had to stop the study early; 28.5% of the placebo group relapsed. The relapses in the placebo group were likely due to the nocebo effect. These findings suggest that some patients have non-celiac reactions to gluten and lot of associated symptoms. For other patients, non-gluten components of wheat may be responsible for triggering symptoms in non-celiac gluten sensitivity.

Systemic immune activation due to food sensitivities is an area of growing concern for patients. As research continues to substantiate the harmful physical effects of food reactions, the personalized diets used by Functional Medicine practitioners will become increasingly important for good patient outcomes.

From Institute for Functional Medicine

Psoriasis, my take

Psoriasis is an autoimmune disease of the skin that affects over three percent of population (that’s about five million adults), and typically involves scaling and inflammation. Psoriasis is a complex autoimmune inflammatory disease that occurs in genetically susceptible individuals and presents with the development of inflammatory plaques on the skin. It has patches of thick red silvery scales that usually itch and hurt. It can affect toe nails, fingernails, joint inflammation causing arthritis.. Some comorbid conditions occur at a higher frequency, include cardiovascular disease, malignancy, diabetes, hypertension, metabolic syndrome, inflammatory bowel disease, serious infections, and other autoimmune disorders. Altogether, it makes for an absolutely miserable experience.

Many times doctors recommend immunity suppressing drugs to calm inflammation. The problem with current medical approach is to look at this condition as a standalone, individual condition and treat as one.

One of the examples of Psoriasis
One of the examples of Psoriasis

For last many years I am looking at conditions with functional medicine principles and looking at the bigger picture. Rather than focusing on the symptoms alone and genes alone, start focusing on causes of symptoms and interactions of genes and environment (the epigenetics) . It is fundamentally a different approach.

That approach is to know the person from all aspects of and all phases of their life to create a health story line specific for that person. That gives better understanding about how that person happens to get this condition. Once you know that you can decide on specific plan for that person.

As per national psoriasis foundation- What triggers psoriasis?
Psoriasis triggers are not universal. What may cause one person’s psoriasis to become active, may not affect another. Established psoriasis triggers include:


Stress can cause psoriasis to flare for the first time or aggravate existing psoriasis. Relaxation and stress reduction may help prevent stress from impacting psoriasis.

Injury to skin</FONT COLOR>

Psoriasis can appear in areas of the skin that have been injured or traumatized. This is called the Koebner [KEB-ner] phenomenon. Vaccinations, sunburns and scratches can all trigger a Koebner response. The Koebner phenomenon can be treated if it is caught early enough.

Medications</FONT COLOR>

Certain medications are associated with triggering psoriasis, including:
Lithium:</FONT COLOR> Used to treat manic depression and other psychiatric disorders. Lithium aggravates psoriasis in about half of those with psoriasis who take it.
Antimalarials:</FONT COLOR> Plaquenil, Quinacrine, chloroquine and hydroxychloroquine may cause a flare of psoriasis, usually two to three weeks after the drug is taken. Hydroxychloroquine is the least likely to cause side effects.
Inderal:</FONT COLOR> This high blood pressure medication worsens psoriasis in about 25 percent to 30 percent of patients with psoriasis who take it. It is not known if all high blood pressure (beta blocker) medications worsen psoriasis, but they may have that potential.
Quinidine:</FONT COLOR> This heart medication has been reported to worsen some cases of psoriasis.
Indomethacin:</FONT COLOR> This is a nonsteroidal anti-inflammatory (NSAID) drug used to treat arthritis. It has worsened some cases of psoriasis. Other anti-inflammatories usually can be substituted. Indomethacin’s negative effects are usually minimal when it is taken properly. Its side effects are usually outweighed by its benefits in psoriatic arthritis.

Infection</FONT COLOR>

Anything that can affect the immune system can affect psoriasis. In particular, streptococcus infection (strep throat) is associated with psoriasis. Strep throat often triggers the first onset of psoriasis in children. You may experience a flare-up following an ear ache, bronchitis, tonsillitis or a respiratory infection, too.
It’s not unusual for someone to have an active psoriasis flare with no strep throat symptoms. Talk with your doctor about getting a strep throat test if your psoriasis flares.

One of the things psoriasis is linked to is increased intestinal permeability (leaky gut). The biggest culprits for that are:

– Heavy metal exposure,
– Dysbiosis and yeast and mold over growth in gut
– Gluten sensitivity
– Smoking,
– Some medications like non steroidal anti-inflammatory meds and antibiotics.
– bacterial, viral, parasitic infections.
– Nutritional deficiencies like vitamin D.

What can be done?</FONT COLOR>

As per Dr. Mark Hyman “take away bad and introduce good to restore body’s natural balance and improve immunity”. Following recommendations are helpful.
-To try to heal psoriasis without use of steroids, and invasive treatment products, we should try this approach first under care of someone who is well versed with this approach.
– Remove food allergy, food sensitivity (specially gluten and dairy) and follow sugar free diet.
– Remove inflammatory diet-and eat organic Non GMO whole foods, wild fish with good omega 3 sources, multi-color fruits and vegetables like berries, orange ,sweet potato, nuts.
– Seek medical help to look all the triggers mentioned above
– As you realize gut plays major role in skin condition, so fix your gut first. Work with functional/integrative physician to optimize your gut health.
– Use the right supplements at right time and right dose. For example fish oil, vitamin D, specific probiotic, anti-inflammatory products like quercetin, turmeric etc. Using anti-inflammatory meal replacement nutritional drink can help people on the go. It is important to follow this plan under physician’s guidance, as they are not free of side effect and complications.
– Regular exercise acts as anti-inflammatory. You just have to go for walks, do outdoor activity like gardening, or take up some sport and then gradually increase to structured exercise.
– Good night sleep-please follows my post on sleep.
– Rest and relaxation-Chronic stress influences inflammation. Calming techniques like meditation, abdominal breathing, yoga, massage, cognitive reflection on your feelings and practicing real gratitude can reduce anxiety and promote calm. You can refer to my post on gratitude, rest and relaxation.

Psoriasis is difficult condition to live with, but there is solution!

Biotoxin mold

biotoxin mold
biotoxin mold

The awareness of toxic mold’s effect on human health has increased dramatically over the past few years. Mold is only one of the many biotoxins found in our environment, and the illness caused by exposure to these toxins is much more complex than most clinicians and patients assume.
Toxic burden is determined by two factors: the levels of toxic chemicals and microorganisms that we’re exposed to, and the function of our innate detoxification system. If toxic burden is higher than our bodies ability for detoxification,( which is determined by our genetic predisposition, epigenetic effects on gene expression, physiologic state of our body and nutrition among other factors) toxins will have adverse effect on our health.
Toxins that affect our health adversely include –Heavy metals like mercury, lead, arsenic cadmium, –Chemicals such as pesticides BPA, endocrine disruptors, fire retardants etc.,
—Biotoxins and biotoxin producing organic organisms are
• Fungi
• Bacteria (possibly including Borrelia, Babesia, and other organisms transmitted by tick bites)
• Actinomycetes (gram-positive bacteria from the order Actinomycetales)
• Mold
• Mold spores
• Endotoxins (aka lipopolysaccharides, or LPS; cell wall components of gram-negative bacteria)
Nearly everyone will become ill when exposed to sufficient levels of these biotoxins, but most people recover once they are removed from exposure. Their detoxification system is able to recognize the biotoxins in their bodies as toxins and eliminate them via the normal mechanisms.
As Dr Shoemaker, who is actively involved in raising the awareness about Mold illness, correctly describes Mold illness as chronic inflammatory response syndrome-CIRS.
Some of the symptoms are:
• Fatigue, weakness
• Post-exertional malaise
• Memory problems, difficulties with concentration and executive function
• Disorientation and confusion
• Headaches
• Vertigo, lightheadedness
• Muscle aches, cramping, joint pains without inflammatory arthritis
• Hypersensitivity to bright light, blurred vision, burning or red eyes, tearing
• Cough, asthma-like illness, shortness of breath, chronic sinus congestion
• Air hunger or unusual shortness of breath at rest
• Chronic abdominal problems including nausea, cramping, secretory diarrhea
• A propensity to experience static shocks
As you can see, these symptoms are “non-specific,” which means that they don’t conclusively identify CIRS (or any other disease) by their mere presence. That is the reason these symptoms are frequently misdiagnosed.
There is HOPE!. Functional medicine way of approaching and evaluating these symptoms has helped patient to come back to vitality and health.