Category Archives: Blog: Diabetes

Weight and Avocados (Replace Refined Carbs with Half or Whole Avocado)

Summary: Few studies look at the role of nutrient combinations (particularly fat and fiber) to enhance satiety. With avocados the rage now, many wonder about the impact on their waist from eating avocados because they are high in fat. What most don’t realize though is that avocados are inherently rich in fiber and that fiber/fat combo should remind you of another functional food (i.e., nuts) which have loads of documented health benefits! Spoiler alert: If you haven’t begun yet to add avocados to your meal, read on. This newly published study found that those replacing refined carbohydrates with fat and fiber (from avocado), as part of a meal, felt significantly less hungry and more satisfied after 6 hours, compared with those who ate a low-fat, high-carbohydrate meal. Spoiler alert: They also found that this group had a healthy metabolic hormonal response, and that combo can help mitigate overweight and obesity! In other words, isocaloric dietary manipulation with a whole avocado promotes favorable metabolic responses in addition to enhancing satiety and reducing motivation to eat. This study was a randomized three-arm crossover clinical trial, [Zhu et al 2019], and it published in the journal Nutrients. The researchers looked at how meals that SUBSTITUTE a half or whole fresh avocado for refined carbohydrates affects hunger and meal satisfaction both subjectively and physiologically over 6 hours, in overweight and obese adults. Many of us are eating low-fat, high-carbohydrate meals so from a practical standpoint, the population studied represents a typical cohort of middle-aged people at risk for cardio-metabolic disease—a point when realistic dietary changes can make a significant impact on reversing the disease risk trajectory. The cohort, N=31, was relatively healthy overweight or obese volunteers having elevated fasting insulin concentrations with insulin resistance [27]. Listen up –> The important physiological implications learned from the study was that the addition of avocado limited insulin and blood glucose excursions, and this correlated with an intestinal hormone called PYY which is an important messenger associated with the physiological response. What that means is that this study provides more evidence that adding healthy fats and fibers into a regular daily diet can modulate blood sugar and insulin spikes and that can reduce the risk of diabetes and cardiovascular disease. Britt Burton-Freeman, Ph.D., the senior study author and director of the Center for Nutrition Research at Illinois Tech said, “The responses on the different satiety variables was surprising and helps us understand [or] think about how the fat and fiber may work to enhance satiety, even later, in the post-meal period.” End-game thought: E- A -T AVOCADOS in place of the refined carbs!

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Intervention Diet Weight Loss Study

Summary:  It is NOT calories in, calories out.  This Intervention Diet Weight Loss Study is looking to show just that.  It is being conducted by five prestigious universities:  Framingham State University, Boston Children’s Hospital, Indiana University Bloomington, University of Alabama at Birmingham, and Baylor University!  The study evaluates the effect of dietary carbohydrate and sugar consumption independent of energy content on body fatness and metabolism in a rigorous feeding study.  The study looks at WHY diets high in total carbohydrate, with or without added sugar, acts through increased insulin secretion, all during substrate partitioning towards storage and body fat, leading to increased hunger, slower metabolism, and accumulation of body fat. This is a randomized controlled feeding study involving 128 adults with BMI between 27 to 40.  The test diets include very low carbohydrate (about 70% fat), High carbohydrate low sugar (25% fat, 0% added sugar), and high carbohydrate high sugar (about 25% fat, 20% added sugars).  

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IBS, Microbiome, Fodmaps, Probiotics

SUMMARY:   Bottom Line of this post: You want OFF the IBS diseasepan!  WHY? Because — putting aside pain, bowel issues, and bloat — IBS can alter the brain size and function in the emotion and sensory processing areas when having it a long time along with early life stressors [Labus et al., 2017], it is associated with A LOT of diseases, and there are A LOT of surgeries performed inappropriately because of misdiagnosis or poor manangement of IBS!  DISEASES that are associated with IBS  — the listing is NOT  comprehensive — includes:   Type 2 Diabetes, metabolic syndrome, fibromyalgia, chronic fatigue syndrome, IBD, CFS/ME, autism, anxiety, depression, MS, and Parkinson’s.  Inappropriate SURGERIES occurring due to IBS  misdiagnosis includes —  appendectomy, cholecystectomy, ovarian, and hysterectomy.  See below for All of those links. There are lots of ways to get off the IBS diseasespan!  Learn in this post that it is YOUR choice:  IBS, Microbiome, Fodmaps, Probiotics, Mindfulness-based stress reduction, Cognitive behavioral therapy works… or targeted drugs!  Or not drugs — because of the poor efficacy of that current US standard of care: =&2=&“The physician should also emphasize the chronic nature of this syndrome [IBS] because nearly 75% of patients continue to have a diagnosis of IBS 5 years later.13  [Occhipinti et al., 2012].   Many different drugs have been suggested for IBS treatment, but their real benefits are very debatable.”  [Bellini et al., 2014].   Don’t be surprised.  In 2012, the FDA changed the endpoints of those drug studies to stop being only one endpoint because of how multi factorial IBS symptomolgy is, and the Bristol Stool Chart — defining what is a ‘normal BM’ (which you’ll learn in this post) — despite being around since 1997, is only now being validated, 2016!  Contrast all this to the UK British Dietetic Association guidelines for IBS — low FODMAP diet is the second-line intervention [Catassi et al., 2017]  [McKenzie et al, 2016]   [UK evidence-based practice guidelines for dietetic management of IBS in adults 2012 PDF])=&2=&as it helps about seventy-six percent of IBS patients  [Magge et al., 2012]  [Bohn et al., 2015]   [Staudacher et al., 2011] and yet, it has come under attack with the current US standard of care still NOT recognizing the FODMAP diet (see this post).  A rebuttal to all the rift recently published in 2017, authored by Monash University ressearchers, the creators of the FODMAP diet.  See  [Hill et al., 2017]  To piggyback the diet fix, studies continue to find that probiotics might be something to think about for some cases of IBS — see  [Whiteley, 2016].  Wondering about IBS and what early life stressors might mean?  That group had more history of early life trauma (general trauma (31 items), physical (9 items), emotional (7 items), and sexual abuse (15 items)) AND they had longer duration of IBS symptoms.  [Labus et al., 2017]  While we can’t change our early life stressors, there are lots of ways to tackle IBS using diet, probiotics, mindfulness-based stress reduction, cognitive behavioral therapy and targeted drugs — according to the Monash rebuttal [Labus et al., 2017].  Now you know!  Protect brain size and function, avoid potentially needless surgery and improve your disease status by fixing IBS; LISTEN to your gut!  Unbelievable… check out the global prevalence of IBS:

DON’T OVERLOOK THE COMMENT SECTION to this post, it adds STUDIES PUBLISHING AFTER I WROTE THIS POST!

IBS is not a condition to ignore.  

Address it & Resolve it considering:  Diet (Fodmaps or similar and probiotics), mindfulness, cognitive behavioral, and/or target drugs because…
  • Many diseases, including those crossing the blood-brain-barrier, are associated with the condition, and resolution of the IBS may help prevent or mitigate the disease,
  • There are a lot of inappropriate surgeries performed due to misdiagnosis (or poor management) of IBS, and
  • It alters the brain emotion and sensory processing areas for those having IBS long term with early life stressors.
Great animation: What is IBS [Monash University]

Most people don’t even realize their symptoms are IBS — and yet IBS affects up to 10 to 25% of the population, and that has a large margin of error since few get counted via physician visits and the inclusion criteria differs. [Canavan et all., 2014].  I always recommend to jounal!

Links to the IBS Disease & Surgery Statistics

Most are surprised to learn that many diseases have IBS associations.  Just to put that into perspective, 30–50% of patients diagnosed with IBD [endoscopically in remission] also report IBS-type symptoms.3, 4, 5.  [Ballou et al., 2017].   Check out the list of diseases having known IBS associations — it is not a comprehensive listing:  Type 2 Diabetes  “Given the higher prediabetes occurrence in IBS, IBS may indirectly indicate a higher risk of Type 2 Diabetes.” [Gulcan et al., 2009], metabolic syndrome “The findings suggest that the treatment of irritable bowel syndrome may be a potentially beneficial factor for the PREVENTION  of metabolic syndrome.”  [Guo et al., 2014],  fibromyalgia (49% have IBS), chronic fatigue syndrome (51%), temporomandibular joint disorder (64%), and chronic pelvic pain (50%) [Heitkemper et al., 2015]IBD [Halpin et al., 2012], CFS/ME [Whiteley, 2017], autism [Navarro et al., 2016], anxiety  and depression [Fond et al., 2014see pdf here, Multiple Sclerosis [Marrie et al., 2015], and Parkinson’s [Mishima et al., 2017].

IBS is complex and multifactorial.  It is “a disruption of the so called “brain-gut axis” that determines changes in the digestive motility and secretion, visceral hypersensitivity, abnormalities of enteroendocrine and immune systems, genetic factors, infections, alterations of the intestinal microbiota and inflammation could play a role in IBS.”  [Bellini et al., 2014].

IBS costs society in terms of medical and loss work absenteeism over $21 billion annually. [Canavan et al., 2014]  As well,  more women (60 to 65%) are affected then men [iffgd, 2016], and lots of inappropriate surgeries due to misdiagnosis occur for IBS suffers.  Some examples include appendectomy, cholecystectomy — 2 to 3 x more likely,  and ovarian  and hysterectomy (twice as likely) occurs 45 to 55% more often in IBS then controls. [=&4=&] [iffgd 2016] [Corazziari et al., 2008].

AND What is a Normal BM?!?

Wondering if you have IBS?  Well.. what does a normal BM look like?  Use the Bristol Stool Chart (BSC) — see TWO versions on the above journal pic — a ‘NORMAL BM’ is rated 3 to 5!  IT FIRST PUBLISHED 1997 [Bristol Stool Chart 1997 PDF], BUT WAS ONLY VALIDATED FOR USE IN THE US IN 2016 BECAUSE IN IBS DRUG CLINICAL TRIALS, “There is little published evidence of efficacy for the most commonly used treatments. Thus, there is an urgent need to conduct clinical trials on existing and novel therapies.”  See [Blake et al, 2016]  [Saps et al, 2016].  If still confused on what is ‘normal’, CHECK OUT A MODIFIED BSC VERSION AT [Lasch et al, 2016].  Honest… I am not making this up… validating the BSC in the US became a scramble because the [FDA Guidance, 2012} changed the “endpoints for clinical IBS trials since prior studies looked at one endpoint which can’t adequately report patient perspective of the complex IBS symptomology”!

The IBS Microbiome Study including early life stressors

The study: [Labus et al., 2017] Differences in gut microbial composition correlate with regional brain volumes in irritable bowel syndrome.

Cohort:  29 IBS adult patients and 23 healthy controls.  Yes, the small cohort is a limitation of the study but as the study concludes: “the correlations of abundance of certain microbial taxa with early adverse life events and with distinct brain structural changes previously reported in IBS suggest a possible role of gut microbes and their metabolites in the development and shaping of the gut-microbiota-brain axis early in life, confirming results from a previous study [10]... Identifying IBS subgroups based on gut microbiota, their related metabolomic profiles and corresponding brain signatures is likely to play an important role in optimizing therapies in IBS.”

Questionaires used for early life stressors:

  •  For background, in mice, early maternal separation induced the brain differences with consequent symptoms similar to IBS [Palma et al., 2015].  Moving to humans, the microbiome/IBS study  [Labus et al., 2017] used The Hospital Anxiety and Depression Scale [HADs] [22], the Patient Health Questionnaire-15 [PHQ] for mood  [23], and the Early Traumatic Inventory–Self Report (ETI-SR) [24] for histories of childhood traumatic and adverse life events that occurred before age 18 years old covering four domains: general trauma (31 items), physical (9 items), emotional (7 items), and sexual abuse (15 items) [24].  Details on the ETI-SR are in the reference section at [Bremner et al., 2011].
  • The Catastrophizing subscale from the Coping Strategies Questionnaire assessed levels of catastrophizing [25]. The degree to which subject viewed situations as stressful in the past month was measured by the Perceived Stress Scale [26].
  • Medication usage included any of the following: antispasmodic, laxatives, stool softener, fiber supplement, nonsteroidal anti-inflammatory drugs, aspirin, acetaminophen, thyroid medications, antihistamine, or proton pump inhibitors.  [Note… PPIs have a disrupted microbiome — see this post.  The significance is that drugs likely need further stratification when evaluating microbiome.]

Findings:  The IBS microbiomes clustered into two subgroups with those having early childhood trauma clustering together.  This trauma could be influencing how the microbes in our gut interact with our brains as we grow, demonstrating a two-way street between the development of our nervous system and the microscopic residents of our digestive system.

  • One subgroup of IBS was indistinguishable from the healthy control cohort.
  • The other IBS subgroup differed and had an altered gut microbiota.  As well, an area of the brain associated with pulling together the body’s sensory information was slightly bigger in this group. The front part of the insular cortex – an area associated with keeping certain body functions in balance as well as dealing with emotions and cognitive functions  was slightly smaller as was the ventral prefrontal regions.  This cohort also had more history of early life trauma based on a psychological evaluation called the Early Traumatic Inventory–Self Report (ETI-SR) Inventory, and a longer duration of IBS symptoms.  “A history of early life trauma has been shown to be associated with structural and functional brain changes and to alter gut microbial composition. It is possible that the signals the gut and its microbes get from the brain of an individual with a history of childhood trauma may lead to lifelong changes in the gut microbiome. These alterations in the gut microbiota may feed back into sensory brain regions, altering the sensitivity to gut stimuli, a hallmark of people with IBS.”  — Gut microbes linked to brain structure in people with irritable bowel syndrome, May 2017 UCLA Newsroom article.  It was postulated that different kinds of bacteria in the gut could be producing chemicals that influence the brain’s development during childhood. Traumatic experiences early in life could affect the brain, which in turn influences the kinds of microbes that grow in the gut. These in turn could influence the brain’s development”. Bacteria Could Be Responsible For Shifts in Brain Structure in People With IBS, ScienceAlert May 2017.

Future — IBS clinical therapeutics

Your Choice:  IBS, Microbiome, Fodmaps, Probiotics, Mindfulness-based stress reduction, Cognitive behavioral therapy and/or targeted drugs?!?

Part 1:  Diet (Fodmaps & Probiotics)

“Analysis of a person’s gut microbiota may become a routine screening test for people with IBS in clinical practice, and future, therapies such as certain diets [low FODMAPS perhaps  [Occhipinti et al., 2012]] and probiotics may become personalized based on an individual’s gut microbial profile.” [Labus et al., 2017]

Diet (Fodmaps)

  • What are FODMAPs?  FODMAPs are food substrates that are poorly absorbed and therefore fermentable by the gut microbiota. The acronym stands for Fermentable Oligo-, di-, Monosaccharides And Polyols. FODMAP substrates are ubiquitous prebiotics in the diet that are difficult to digest for everyone, they are additive, and when in excess for your unique physiology, can cause digestive symptoms.  There is an accumulating body of evidence, based on observational and comparative studies, and on randomized-controlled trials that supports the notion that FODMAPs trigger gastrointestinal symptoms in patients with functional bowel disorders.” [Shepherd et al., 2013].
  • The FODMAP diet is not intended to be long-term therapy.  From Monash University (the creator of the Low FODMAP diet):  A low FODMAP diet will reduce the intake of foods high in fibre and natural prebiotics, which in turn may impact of the growth of certain bacteria in the gut.  This is why we advise against following a strict low FODMAP diet  unnecessarily.  Typically consume low FODMAP 2-6 weeks, then re-introduce FODMAPs in a deliberate process to learn tolerance levels using a FODMAP knowledgeable professional.” Source: Monash University, Dietary Fibre and natural prebiotics for gut health: FAQs.   The below chart lists some prebiotic FODMAPs that beneficially feed the microbiome.
  • A FODMAP re-introduction guideline can be found at:  Metagenics, Patient Information: Low FODMAP Diet for Irritable Bowel Syndrome
  • The efficacy of the elimination phase of the low-FODMAP diet for overall gastrointestinal symptom relief in adult patients with IBS has been seen in randomized, controlled trials; a blinded, randomized, rechallenge study; and observational studies that have been reviewed in detail elsewhere3,4 as well as in a meta-analysis.5 These studies have shown that 50% to 86% of patients have a clinically meaningful response to the low-FODMAP diet. In contrast, the success of maintenance (the reintroduction phase of the diet) has been studied less (in only a few observational studies).6,7 Due to the difficulties of designing an appropriately blinded, randomized, longer-term, interventional study, the evidence base for maintenance will likely remain less solid. [Hill et al,, 2017],
  • Dr. Gibson, the creator of the FODMAP diet, estimates that overall ~10% of the population may be FODMAP-sensitive.  The book, The Complete Low-FODMAP Diet: A Revolutionary Plan for Managing IBS and Other Digestive Disorders, by Drs. Sue Shepherd and Peter Gibson is a reference guide and road map for the low-FODMAP diet.
  • Figure out if it is Gluten or FODMAP Intolerance!  The FODMAP gold standard of food intolerance testing (ie, food exclusion to achieve symptom resolution followed by gradual food reintroduction and subsequent symptom induction to identify tolerance)35 is important because often gluten is not the dietary culprit contrary to many thinking otherwise.  “Randomized studies have shown that there is a lack of gluten specificity in the induction of symptoms in the vast majority of patients with self-reported NCGS.3234   Another trial of 36 patients experienced improvement in gastrointestinal symptoms when placed on a low-FODMAP diet during the run-in period, but none had repeatedly consistent exacerbation of symptoms specifically on ingestion of FODMAP-depleted gluten during the blinded rechallenge phases.31 One logical interpretation of these studies is that the FODMAP reduction associated with avoidance of wheat, rye, and barley—all high in FODMAPs—led to partial response, and more extensive FODMAP restriction further improved that response.”  See  [Hill et al,, 2017] for reference links.
  • IBS, Food Intolerances, and SIBO.  FODMAPS may work since 75.6%, 37.8% and 13.3% of  [IBS] patients had fructose, lactose malabsorption or small intestinal bacterial overgrowth respectively.  [de Roest et al 2013]  [Barrett et al., 2007].
  • Disease and FODMAPs — IBD.  The FODMAP diet successfully manages over 86% of IBS/IBD patients, having partial (54%) or full (32%) efficacy.  Satisfaction with dietary management was seen in 83 (70%) IBS patients and 24 (55%) IBD patients. Eighty-four percent of patients lived on a modified low FODMAP diet (LFD), where some foods rich in FODMAPs were reintroduced, and 16% followed the LFD by the book without deviations. WHEAT, DAIRY products, and ONIONS were the foods most often NOT reintroduced by patients. [Maagaard et al., 2016].
  • Disease and FODMAPs —Diabetes.  The Joslin Diabetes Center, a teaching and research affiliate of Harvard Medical School, recommends trying FODMAP for diabetes! Have IBS [and Diabetes]? Try FODMAPs.
  • Genetic predisposition and IBS. There may be a subset of patients that are genetically predisposed to IBS due to mutations in the gene encoding the enzyme sucrase-isomaltase which is responsible for the digestion of small carbohydrates from sugars and starches called disaccharides.  15Phe is a common sucrase-isomaltase polymorphism. “A significant decrease in the enzymatic activity of sucrase-isomaltase would be compatible with poor carbohydrate digestion in the intestine, possibly leading to malabsorption and bowel symptoms,” Hassan Naim, PhD.  [Henström et al,, 2016] and see this Healio article. 
  • Fructose and children under 10 years age:  “Children under the age of 10 years have a reduced capacity to absorb fructose. It would be important to assess whether young children with IBS are consuming a high-FODMAP diet with excessive amounts of fruit/fruit products, dairy/dairy products, and wheat/wheat products. Furthermore, it would also be important to assess whether normalizing—that is, limiting portions of fruit, dairy, and wheat to reduce dietary intake of FODMAPs—results in symptom resolution.”  [Hill et al., 2017]

Probiotics — They Work Well for IBS!

The study.  [Zhang et al., 2016]   Meta analysis of 21 randomized controlled trials (RCTs) that compared  many probiotics including different types of Lactobacillus acidophilus and Lactobacillus rhamnosus  including  VSL#3 with placebo.

Conclusion:  “Probiotics are an effective pharmacological therapy in IBS patients.  Single probiotics, a low dose, and a short treatment duration were more effective with respect to overall symptom response and quality of life.”  Some probitoic(s) worked very well but we don’t know enough about which ones used under which circumstances because the authors did not analyze “the effects of individual probiotic species”.

Practically,  Try many different whole food probiotics. You’ll find those in the refrigerated section, or try making your own and see how you feel — see my Pinterest Ferment Board for starters.  Always start     S—L—O—W!   Here is the link for how I make SCD Yogurt – the FODMAP lactose is eliminated in this recipe since the long ferment time renders the yogurt lactose-free.  Regarding the inflammatory casein protein, it is said that the recipe changes the protein to more digestible, but different milks can also be trialed to decrease the inflammatory nature of casein. If you find you still cannot tolerate yogurt, try non-dairy ferments such as those in the below pic.  Note too:  You should try those non-dairy ferments anyway because all ferments contain differing probiotic bacteria and more is better when it comes to talking microbiome diversity.

Part 2:  Mindfulness-based stress reduction, cognitive behavioral therapy and/or targeted drugs?!?

Intro:  Health psychology and gastroenterology have become increasingly aligned over the last several decades because: There is strong evidence that cognitive behavioral therapy; hypnotherapy; and mindfulness-based therapy directly target physiological processes by reducing arousal of the autonomic nervous system, decreasing the stress-response, and even reducing inflammation. This physiologic effect is largely due to the so-called brain-gut axis, which explains in part the common gastrointestinal consequences of stress and anxiety. Although the brain-gut axis is particularly important in the treatment of IBS [and ALL diseases having IBS associations], it is also relevant among patients with IBD, especially when considering the increased likelihood of an IBD flare in the context of chronic stress.84, 85 ”  [Ballou et al., 2017].

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Type 2 Diabetes, diet, microbiome

Summary:  Say you use to have Type 2 Diabetes.  How?  READ this study from ITALY.  Ma-Pi 2 diet for Type 2 Diabetes WORKED.  Type 2 Diabetes, diet, microbiome; the Ma-Pi 2 diet for Type 2 Diabetes is dietary modulation of microbiome.  Although this diet BEAT the current recommended diet by Italian professional societies (CTR) consider using it short term and supplementing the diet similar to recommendations by Drs. Mark Hyman and David Ludwig noted below, with healthy fat, wild caught fish, berries, and fermented dairy (if tolerated), since the restriction of certain groups could lead to nutritional deficiencies especially vitamin B12 and calcium.   Actually, Dr. Hyman just offered his 10 Day Detox diet for FREE to the public that clarifies all the food recommended.  You can read about that at the post, JOIN DR. MARK HYMAN FREE 10 DAY DETOX CHALLENGE.  You may still be able to take advantage of this opportunity.  To clarify the carb loads for diabetes, Dr. Ruby Aujla’s Advice to Diabetes page (which is 100% in accord with Dr. Hyman’s 10 Day Detox) says,  Get your carbs from colorful plant based sources.  Even breakfast should be brimming with those!  Bread, White Rice, Pastas, White potato, Cereals (even cereals marketed as ‘wholegrain’), Instant Oats, Refined Grains, white potato are OUT.”  The Ma-Pi2 study describes in pain staking detail, microbiome wise, microbiome impact.   Talk with your doctor for Ma-Pi 2 integration with therapy.  Managing the microbiome through diet is new, grassroots, and it works.   SAVE a friend and SHARE this post. 

Type 2 Diabetes, diet, microbiome

Ma-Pi 2, but NOT the CTR, counteracted increase of possible pro-inflammatory microbiome species

This is a major difference!  Ma-Pi 2, but NOT the CTR, counteracted increase of possible pro-inflammatory microbiome species, showing the potential to reverse pro-inflammatory dysbioses in T2D, and possibly explaining the greater efficacy in improving the metabolic control.  You already know:  The foods you eat pre-selects your microbiome comunity!  Think of it as your microbial passengers seeing a lot of sugar from the boatload of starch and sugar you eat… those microbial passengers are looking for the missing antioxidants (from berries and EVOO for example), the missing phytonutrients and phytochemicals (from vegetables, fruits…), and etc.  Feed them what they need to flousish beneficially and you’ll see weight, waistline, and increased energy results!

Ma-Pi 2 was more effective then CTR in reducing fasting and postprandial blood glucose, glycated Hb (HbA1c), serum cholesterol, homeostasis model assessment of insulin resistance (HOMA-IR), BMI and waist and hip circumferences compared with the CTR diet.

What is the Ma-Pi 2 Diet?

Ma-Pi 2 is complex carbohydrates, legumes, fermented products, sea salt and green tea, and it excludes fat and protein from animal source and added sugars. 

My preliminary research on what exactly is the MA-PI 2 diet gives pause; the restriction of certain groups could lead to nutritional deficiencies especially vitamin B12 and calcium.   Think about using Ma-Pi 2 short term and of supplementing the diet with healthy fat, wild caught fish, berries, and fermented dairy similar to recommendations by Drs Mark Hyman and David Ludwig:  

Updated 10/23/2016:  The fat/carb loads are confusing.  The bottom line is that all calories are not alike.  Dr. Mark Hyman, Cleveland Clinic, has an incredible YouTube summary of the macronutrient balance for fat intake at  Why Fat Doesn’t Make You Fat!  Another favorite researcher is Dr. David Ludwig.  One of my favorite posts of Dr. Ludwig’s is at: Dr. David Ludwig clears up carbohydrate confusion. An important excerpt:  

… highly processed [refined grain, for example,] rice cereal [so much for those going gluten-free and choosing Cheerios] and table sugar may taste different, but below the neck they both cause metabolic problems.  The distinction between sugar and starch is largely meaningless from a biological perspective. The key public health challenge today is to reduce intake of all highly processed carbohydrates in favor of whole carbohydrates (fruits, vegetables, legumes and minimally processed grains) and healthful fats (like nuts, avocado and olive oil).

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Heartburn drugs, dementia, Alzheimer’s risk for all? T2D, is it the canary in the coal mine!?!

   Fire in the gut is fire in the brain — Dementia, Alzheimer’s.  SUMMARY:  A recent study found risk of dementia in PPI users aged 75 and over.  Previous studies had found that Histamine H2 antagonists (H2RAs) also have adverse cognitive impact in the elderly but the mechanism differed… it was due to anticholinergic effects; I wrote about that here. Can the heartburn drugs, dementia, Alzheimer’s risk associations be extended to younger ages?

What may be possible mechanisms?  This post lists the PubMed studies finding that heartburn drugs put fire in the gut; they 

  1. Skew microbiome — PPIs microbiome skew is so severe it increases the risk of CDiff and HALF of users have small intestinal bowel overgrowth, aka SIBO.  Regarding the H2RA impact on the microbiome, there is only a paucity of data  though studies are now ongoing. However, given that it too is an acid reducer,  microbiome impact is likely similar to PPI.  And
  2. Both PPIs and H2RAs mug nutrients, especially B12 which is associated with cognition.

Both of these mechanisms are not age dependent.  “Fire in the gut is fire in the brain”.   

With dementia known to be associated with B12 deficiency, and if dementia is shown to be associated with microbiome skew in humans, (this mouse study also suggests such) are heartburn drugs (that skew microbiome and deplete B12), dementia, Alzheimer’s a risk for all ages?  Can impaired cognition for Type 2 Diabetes (T2D) irrespective of age, many of whom also take acid reducers, be the canary in the coal mine suggesting YES?  Read on; it may be time to re-think grandma, your dad, yourself, and your child on heartburn drugs.  

Last, this post shows another mechanism for dementia for all ages — high blood sugar with or without diagnosed diabetes Diet guidance (with links) that lowers blood sugar for all is provided. 

Realize however, dementia and Alzheimer’s risks are multi-factorial. It is certainly worth reducing their risk by focusing on risk factor associations.

Some confounding factors for cognition risk includes exercise and here,  cardiovascular gut microbiome impact (mouse study) and diet this post details optimal microbiome diet learned thus far from American Gut though not specifically addressing brain health, or possibly even overgrowth of oral anaerobes in the brain. The later is challenging the entrenched dogma that organs are supposed to be sterile.  For example, bacterial findings in the placenta  and amniotic fluid is thought to likely be a natural part of in utero development with the hypothesis that exposure to harmless bacteria “trains” the developing immune system — however, bad things may happen to this taxa and overgrowth is one thought.  For another example see the breast microbiome — cancer post).  Actually, the greatest known risk factor for Alzheimer’s is the aging brain; it certainly makes sense to knock down all the risk factors that one can

lightbulb2If gut microbiome is found to be associated with dementia, reducing/eliminating the acid reducer factor which is contributing to skewed microbiome, with physician guidance, knocks down a big contributor to microbiome skew. Check out Dr. Mark Hyman’s post here to begin to self educate yourself on reducing heartburn drugs.  

We now know that acid reducers are associated with cognition impairment in the elderly.

The study:  Association of Proton Pump Inhibitors With Risk of Dementia A Pharmacoepidemiological Claims Data Analysis, published Feb, 2016 in JAMA, reports on increased risk for dementia for PPIs in older patients.  See also the associated MedScape article, Proton Pump Inhibitors Linked to DementiaIn the study, Regular PPI use was defined as at least 1 prescription per quarter for: omeprazole, pantoprazole, lansoprazole, esomeprazole, rabeprazole.

Results  A total of 73 679 participants 75 years of age or older and free of dementia at baseline were analyzed. The patients receiving regular PPI medication (n = 2950; mean [SD] age, 83.8 [5.4] years; 77.9% female) had a significantly increased risk of incident dementia compared with the patients not receiving PPI medication (n = 70 729; mean [SD] age, 83.0 [5.6] years; 73.6% female) (hazard ratio, 1.44 [95% CI, 1.36-1.52];  < .001).  The association was slightly more pronounced in men than women (HR 1.52 versus HR 1.42), though both were statistically significant

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Preserve & Restore Loss of Microbiome Diversity is Aggressive Preventative Medicine

SUMMARY:  Aggressive Preventative Medicine means preserving the microbiome you have and restoring any loss incurred.  See how far that thought goes with your doctor!  Diet really does work to alter the microbiome and can help to restore loss of microbiome; for example, fermented kimchi actually positively impacted metabolic syndrome factors including systolic and diastolic blood pressures, percent body fat, fasting glucose, and total cholesterol.  

⇒⇒  This post teaches how to reduce the loss of microbiome diversity and restore such – crowding out concept.

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We see & perceive things differently; Neither is superior to the other

SUMMARY:  The ‘blue/black white/gold dress‘ incident is a really good way of acknowledging that people see and perceive things differently and one way is not necessarily superior to the other.  I see and appreciate this in every diet conversation I have.  I focus a lot on diet; but lifestyle tweaks help many achieve wellness when clean diet isn’t enough.  Initial microbiome studies show that stress can result in changes to the gut microbial community, specifically bacteria in the genus Lactobacillus are consistently reduced.  If clean diet isn’t enough, move onto stress busters that data shows literally reduce inflammatory markers — affirmations and meditation do such.

I use data, and you understand physiologic birth and breast feeding, OTC and prescription drugs like Proton Pump Inhibitors and oral contraceptives, antibiotics, NSAIDs, and about food and their choices: gluten, GMOs, sugar...   I use data and you understand the bi-directional relationship between the gut and brain and body organs… that cytokines are messengers that travel and communicate through the vagus nerve & microglia [a type of glial cell that are the resident macrophages of the brain and spinal cord, and thus act as the first and main form of active immune defense in the central nervous system (CNS)] that they interfere with feedback loops, hormones, immunity, and trafficking of neurotransmitters. I decimate and show false, the boundaries between immunology, autoimmunity, neurochemistry, and endocrinology.  

You understand there is no one magic diet for all as you arrive at your most anti-inflammatory diet based on your own unique genetics, epigenetic alterations, and goals.  But in so doing, how do you deal with that fishbowl feeling, be it with your health care provider, family, friends, or peers?  Affirmation and meditation are incredibly powerful stress busters as they literally reduce inflammatory markers; use them in addition to other strategies  such as exercise, reading, music, fishing, hiking, socializing…. How powerful are affirmations and meditation???

embellishment7Affirmations, meditation, and yoga reduced inflammation-related proteins:   10% lower level of TNF-a,  11% lower IL-6, 15% lower IL-1B,  up to 20% reduction of inflammation, improved sleep, and a 57% decrease in fatigue.  Researchers believe the meditation and breathing aspect was the main contributor to reduced inflammatory markers.embellishment7

The study:  In 200 breast cancer patients who had undergone surgery or radiation treatment, significant inflammatory marker reductions were realized:

Findings for 12 weeks of yoga  (researchers felt breathing and meditation aspects were main drivers of results):  Participants were first injected with a compound that provoked an immune response before giving blood samples.  Average lower levels of the inflammation-related proteins than the controls were: 10% lower level of TNF-a, 11% lower IL-6, 15% lower IL-1B, improved sleep, up to 20% reduction of inflammation, and a 57% decrease in fatigue. The study also showed the more yoga the women practiced, the bigger the improvements in fatigue, vitality, depressive symptoms, accompanied by increased reductions in two of the inflammation-related proteins, IL-6 and IL-1B.

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IBD CAM, LDN, probiotics, SCD… & Integrative Medicine benefits gut health

SUMMARY:   IBD CAM “Probiotics, Special Diets [SCD], and Complementary Therapies:  We Know Patients Want Them, So What Do We Tell Them? was presented at the Dec. 2014  Advances in IBD conference, by Dr. Sandra Kim, MD, who noted, “SO CERTAINLY THERE IS SOME PROMISE IN AT LEAST THINKING ABOUT THIS.”  Now that’s a first!!!  At least one conventional doctor is encouraging her peers to  seriously educate themselves about IBD CAM, LDN, probiotics, SCD… and  Integrative  Medicine and to ask their patients if they are interested in them, using them and if so, what do they use, and to actively seek funding for further study of them!  And… Dr. Kim has disclosure of conflicting interests — Speaker: Nestle NutritionAbbott Laboratories and Consultant: AbbVie Pharmaceuticals!

IBD CAM, LDN, probiotics, SCD:  “Probiotics, Special Diets, and Complementary Therapies:  We Know Patients Want Them, So What Do We Tell Them?(PowerPoint link)

That title (no joking) says it all now, doesn’t it?  But no worries… the conference presentations have always questioned protocols such as the presentation:  Should We Change How We Position Biologics in UC? 

Dr. Kim is a pediatric gastroenterologist; her continuing medical education presentation was fifteen minutes.  No time was left for questions; no surprise there.

embellishment7Bottom line:  there really is disease activity indices improvement and mucosal healing taking place with these modalities.embellishment7

You can watch Dr. Kim’s Presentation in the below YouTube: Probiotics, Special Diets, and Complementary Therapies: We Know Patients Want Them, So What Do We Tell Them?”  Probiotics, Special Diets, and Complementary Therapies:

Dr. Kim addressed ten CAM and Integrative Medicine practices having anti-inflammatory impact and/or decreased disease activity indices on the gut function as it relates to IBD, although it should similarly relate to other gut dysbiosis and may be worth your time to Google research such.

Dr. Kim concluded saying she personally, with patients:
  1. Goes through the medications,
  2. Goes through the nutrition,
  3. Then she is open and up front asking patients if they are interested in different types of integrative medicine practices, or CAMs, and if so, what sorts of practices or supplements they are utilizing.  She stressed to:  LISTEN WITHOUT JUDGEMENT as there is a perception that physicians believe in only the Westernized medicine and judge, and for this reason, often she thinks the families are NOT upfront in the non-Western practices they are doingShe always says it is best to know what patients are thinking!!!  I honestly don’t think they would like to know, at times, strictly my opinion.
  4. She thinks physicians should:
    • Understand the literature or they are not credible.
    • Know how the literature talks about the practice; is it used as primary or adjunct therapy.
    • Know what the benefits and potential downsize is.
Treatments she discussed are:
  1. Artemisia or wormwood found to have a 65 to 80% improvement of disease activity indices; that was better than Remicade,
  2. HMPL found to have beneficial clinical response but not remission at 8 weeks; thought to exert anti=inflammatory effects due to TNF, IL-1β, and NF-kB pathways.
  3. Curcumin plus 5-ASA had 5% relapse versus 5-ASA alone which had a 21% relapse.
  4. Cannabis helped with symptoms but was a greater predictor of progression to surgery (OR 5.03).
  5. LDN improved disease activity indices for Crohn’s.
  6. Probiotics.  The below images also include #7—Prebiotics and #8—SCD.  Dr. Kim acknowledged FMT but decided to not discuss it in this presentation. 

    Probiotics:  Potential butyrate producers.  Some efficacy in pouchitis and  UC but not Crohn’s.  VSL#3 helped post operative surgery Crohn’s.

    • But I am inserting a note:  SCD, eaten for one month at about 80% compliance, was shown to increase F. prausnitzii for IBD Crohn’s; F. prausnitzii is a butyrate and antioxidant producer, and it is found to be reduced in IBD.  See IBD CROHN’S: SCD INCREASED MICROBIOME DIVERSITY BUT LOW RESIDUAL DIET REDUCED DIVERSITY and the study at: Analysis of Gut Microbiome and Diet Modification in Patients with Crohn’s Disease, as well as the post, NICE, EATING SCD INCREASED F. PRAUSNITZII… HUGH?!? which explains the significance of F. prausnitzii in the microbiome.
    • Another great read on F. prausnitzii and IBD is Among Trillions of Microbes in the Gut, a Few Are Special as it suggests perhaps F. prausnitzii, part of the clostridial clusters, that do the opposite of CDiff in a gut they keep the gut barrier tight and healthy, and they soothe the immune system… In East Asian populations the gene variants associated with IBD differ from the gene variants in European populations. Yet the same bacterial species—F. prausnitzii—was reduced in the guts of those in whom the disease developed. This suggested that whereas different genetic vulnerabilities might underlie the disorder, the path to disease was similar: a loss of anti-inflammatory microbes from the gut. And although Sokol suspects that other good bacteria besides F. prausnitzii exist, this similarity hinted at a potential one-size-fits-all remedy for Crohn’s and possibly other inflammatory disorders: restoration of peacekeeping microbes.
  7. Prebiotics did not help significantly in changing typical probiotic strains like bifidobacteria or F. prausnitzii.  But see above study for SCD study that did show this change for IBD-Crohn’s.
  8. SCD (1 year consumption, individual patients are charted):
    • Stan Cohen, 2014 JPGN study: disease activity indices and endoscopic for mucosal healing showed improvement in PCDAI as well as Lewis Scores (measurement of mucosal healing when undergoing capsule endoscopy.)
    • Also Suskind  2014 JPGN study from Seattle Childrens found significant improvement in multiple parameters including albumin and hemoglobins.
  9. Acupuncture in IBD: improved sense of well being.
  10. Hypnosis for IBD:  one 50 minute session had mucosal and serum inflammation markers decrease.

embellishment7“SO CERTAINLY THERE IS SOME PROMISE IN AT LEAST THINKING ABOUT THIS,”  -Dr. Kim embellishment7

While I am happy she included SCD, I am disappointed that she missed a lot of the studies.

Nutrition as Medicine in the past has been a holistic approach by those wanting to avoid medication side effects.  Limited studies have been conducted and most are outside the US.  There is a surprising overlap of IBD and IBS symptoms.  The FODMAPS diet seriously helps over 70% of IBS and has decent research behind it.  See the post, IBS: FODMAPS, STOMACH MICROBIOME & RIFAXIMIN ANTIBIOTIC TREATMENT, SERIOUSLY?!?  Not surprising, many of the SCD type diets used for IBD have FODMAP overlaps.  At times I think this is the concept that keeps diet management of IBD within reach, but it is hampered by the need for conventional physician’s to recant the knee jerk reaction, “Diet has nothing to do with it [IBD]” that patients hear again and again.  And patients need to realize that as in Type 1 Diabetes control, diet management may not be a negotiable concept.  What is sad is the lack of physician understanding that eating SCD is not that difficult, even on the road, once you learn and understand the rationale for its tenets and how to practically implement SCD.

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Microbirth: Health Ramifications associated with C-Section birth

SUMMARY:  Learn the long term health ramifications associated with  C-Section birth.  “Microbirth” information every parent needs to view.

Microbirth is a new 60 minute documentary investigating the latest scientific research about the microscopic events happening during childbirth.  As this Press Release explains, latest research is starting to indicate modern birth practices could be interfering with critical biological processes.   From the changes that occur in the human pregnant vaginal microbiome to that microbiome which actually inoculates the baby, be it via C-section or vagina birth, these  events are now showing to have associated consequences for the health of the child and  such could have life-long consequences making our children more susceptible to disease later in life:

Recent population studies have shown babies born by Caesarean Section have approximately:
  • 20% increased risk of developing asthma,
  • 20% increased risk of developing type 1 diabetes,
  • 20% increased risk of obesity,
  • slightly smaller increases with gastro-intestinal conditions like Crohn’s disease or coeliac disease, and
  • These conditions are all linked to the immune system.

Does C-section cause these conditions?  Dr Rodney R Dietert, Professor oat Cornell University, says, No. What C-section does is not allow the baby to be seeded with the vaginal microbes.”  Proper seeding of the newborn is an important microbiological process where bacteria is transferred from the mother to the baby in the birth canal.  As a consequence, the baby’s immune system may not develop to its full potential.  Dr Dietert expains, “The immune system doesn’t mature, and the metabolism changes. It’s the immune dysfunction and the changes in metabolism that we now know contribute to those diseases and conditions.”  

Another hypothesis presented inMicrobirth:  the stresses and hormones associated with natural birth could switch on or off certain genes related to the immune system and metabolism.  If a baby is born by C-Section, this might affect these epigenetic processes.  Below is the 2 minute MicrobirthYouTube trailer:

Microbirth should be mandatory viewing for every parent, pregnant women, and physician to better understand the need to care for and nurture the microbiome health pre-conception, in utero, in labor, and post delivery.  Matter of fact, I think it should be viewed in school health education classes so that children better understand the need to care and nurture their microbiome.  Who is in the film Microbirth  reads like a who’s who in research, and if you are a reader of my work, you’ll recognize them all:

Who Is In the film "Microbirth"
Source: http://microbirth.com/about/

The Downloads section of the  Microbirth website contains FAQ, which I am excerpting below, to impress upon my readers the need for them to pass on this information:

Q&A On The Science Behind Microbirth: By Rodney Dietert, Professor of Immunotoxicology, Cornell University
  • If a baby is born with the white waxy vernix, will the microbiomes be washed off or come off when the baby is cleaned, as they usually are right away if they are in a hospital setting?  Or, does the newly seeded microbiomes wash off in a water birth?  Don’t know. Not much if anything has been published on this specific factor. Just on vaginal (and what that includes) vs. Caesarean delivery.
  • How fully seeded can a child get after a C-sectionAs a group, C-section delivered babies have a lower diversity of microbes and lower numbers of some useful bacteria types comprising the microbiome than do vaginal-delivered babies. So they are not as fully complete and also their seeded microbiome is less derived from their mother compared with vaginally delivered babies. Treatments such a the use of vaginal swabs at birth for C-section babies may be helpful for self completion.
  • And what or whose microbiomes is a C-section child getting?  The exact range of sources of the C-section baby’s microbiome remains somewhat uncertain. But it is clear that much less of it is from the mother (particularly for gut microbes) than in vaginally-delivered babies. So for C-section babies, much of their seeding is coming from the surroundings (e.g., the hospital environment, hospital personnel, and patients).
  • Are most of the auto-immune diseases coming from C-section born children?  As a group, C-section delivered babies have a higher prevalence of auto-immune and allergic conditions than do vaginally delivered babies. However, birth delivery mode is not the only factor in risk of immune disorders. Exposure of the parents (particularly the pregnant mom) and the baby or infant to toxic chemicals (e.g., heavy metal, plasticizers, pesticides, air pollutants) and drugs and/or to adverse environmental conditions (low vitamin D, stress/abuse) can also produce immune dysfunction and elevated risk of auto-immune and allergic diseases.
  • Are there children with these listed diseases that were born vaginally?  Vaginally-delivered children can and do get auto-immune and allergic diseases. Their families may have genetic predispositions for these diseases and/or they may have exposed either in utero or early childhood to harmful chemicals or drugs that promote these diseases. For example, a mother with extensive heavy metal exposure or who had multiple rounds of antibiotics and delivered vaginally could have a severely depleted microbiome for seeding her baby. However, as a group, vaginally-delivered children have a lower prevalence for these immune disorders than occurs with C-section delivered babies.
  • If so, where do their diseases originate?  Immune and inflammatory disorders such auto-immune and allergic diseases are thought to originate via a combination of family genetics, prior family-related exposures (epigenetics) and current early life environment. The developing immune system is programmed for dysfunction and as the child matures, improper immune-related responses to environmental challenges (e.g., childhood infections) show up as auto-immune, allergic or inflammatory conditions. Because the microbiome helps to train the immune  system as to what is friend or foe, a complete and useful microbiome helps to reduce the risk of these diseases.
  • Has there been a study done regarding this?  Yes. Many studies have examined the causes and triggers of immune disorders such as childhood asthma, type 1 diabetes and celiac disease as well as the role of the microbiome in controlling immune maturation and affecting the risk of these diseases.
  •  Is the young child still getting “microbiomes” if they continue nursing past babyhood?  The young child would still have some exposure to the mother’s microbes that may help to fill in any remaining blanks. However, it is the breast milk that nurtures the gut microbes and helps the baby’s microbiome to mature that is probably the more important factor. Exposure to the microbes early is important because that is when the immune system needs to see the microbes the most for effective immune maturation.
  • If a mother stops nursing after a few weeks, has the baby not been fully seeded? When does seeding stop?  Most seeding occurs during the first year with the majority of that probably occurring during the first few months. However, if the infant has received antibiotic treatments, the microbiome may need to be reseeded at least in part.
  • What about recent research indicating the baby’s microbiome may be seeded before birth?  The film Microbirth” does not say that the only exposure to microbes is at birth. In fact, the film points out prenatal exposure to bacteria and/or bacterial products is likely to occur. But it makes the point that birth and the period surrounding it appear to be the single most important seeding event that:
    1. Determines whether self completion of the infant fully occurs (complete seeding of the microbiome) and
    2. Promotes necessary postnatal immune maturation. If prenatal exposure were adequate for self completion, then C-section-delivered babies would not (as a group) have restricted microbiomes and elevated risk of later–life non-communicable diseases (when compared to the group of vaginally delivered babies)
"Microbirth," Sept 2014, 60 minute film
Source: http://microbirth.com/downloads/
Important posts related to Newborn Microbiome and which contains the study citations/links:
  1. NEWBORN GUT MICROBIOME BEGINS DURING BIRTH
  2. DELIVERY & BREASTFEED STUDIES & MICROBIOME MANIPULATION
  3. 1ST STUDY: LOW DOSE BPA PERINATAL EXPOSURE & FOOD INTOLERANCE

The film’s co-Director Toni Harman says, “The very latest scientific research is starting to indicate that the microscopic processes happening during childbirth could be critical for the life-long health of the baby. We are hoping Microbirth” raises awareness of the importance of “seeding the microbiome” for all babies, whether born naturally or by C-Section, to give all children the best chance of a healthy life. This could be an exciting opportunity to improve health across populations. And it all starts at birth”.  

Now that you’re lucky enough to know… do your own part and pass this post on: to your friends, your Facebook, your twitter, your doctors…  Let’s make this world a better place for its children.

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Testing if calories trigger hormones that regulate fat cell behavior

Summary:  NUSI is now testing if calories trigger hormones that regulate fat cell behavior.  This will help answer the question of  which camp we should we be in, namely:  the sugar is  bad/saturated fat is the good camp versus the whole grain/low fat is the good camp. 

Enter NUSI →   Seems bad science got us into the mess and state of confusion and ignorance.  So Gary Tuabes has aligned with Dr. Peter Attia, MD to do good science and answer the age old question:  Do we get fat because we eat too much and especially too much fat OR is it the food we eat, especially the increased consumption of table sugar and other refined carbohydrates the likely explanation for our current chronic disease epidemic including obesity?  There’s a real difference there, honest!

Disease Epidemic_PNG file
Slide source: biomeonboardawareness.com

Taubes radical alternative hypothesis theory in simpleton:  Condensed from this article:  We get fat NOT because we eat too many calories but because specific kinds of calories trigger hormones that regulate how our fat cells behave. In particular, eating refined carbohydrates, and especially sugar, on a sustained basis leads to chronically elevated insulin levels. Among its many other crucial functions in the body, insulin tells fat cells to take up glucose, which is converted into fat, and then keeps fat from all sources locked inside. Consume a bunch of sugar every day, as most Americans do, and you’ll get fat.

Of course, Taubes could only present the hypothesis. He couldn’t prove any of it. The right experiments had never been done.