Quantified Self Experiments / Science - Health Insights


At this page I'll post some scientific studies related to different health topics which i've found useful and integrate into my life.

My conclusions

Dont trust me, people, friends, broscience, health organisations, experts, books, politics, blogs, mass-media saying something about health without checking primary scientific source by yourself. Most of time there is no evidence, just hype, blind faith, bias and misinformation. Correlation very rarely a causation. P-values often misleading. Even scientific results often not replicating and contradictive. Use Bayes theorem and update your priors after reading new information, avoid confirmation bias and other biases. Read Wrong science section and use critical thinking.

Nutrition & Metabolism

Postmeal glucose response is connected to wide health markers age, BMI, HbA1c%, fasting blood glucose, T2DM. Food adjusting can improve glucose profile and change microbiota in positive direction. Glucose food response may be predicted from microbiota analysis (stool sample). Fat, salt, water, time from waking up and other factors may alter glycemic response.  There were some food caused high glycemic response in most of people (pizza, pita, rice, bread) Cell, 2015

We demonstrate that PPGRs are highly variable across individuals even when they consume the same standardized meals.PPGRs in our study also associated with several risk factors, including BMI, HbA1c%, and wakeup glucose.We report several associations between microbiome features and variability in PPGRs across people. In some cases, such as for Actinobacteria, Proteobacteria, and Enterobacteriaceae, the direction of our associations are consistent with previous associations reported between these taxa and higher-level phenotypes such as dietary habits, obesity and overall glycemic control. Dietary interventions based on our predictor showed significant improvements in multiple aspects of glucose metabolism, including lower PPGRs and lower fluctuations in blood glucose levels within a short 1-week intervention period. 

Fat and carb calories aren't same! Body utilise them with different efficacy. The American Journal of Clinical Nutrition, 2017 

Recorded intake of carbohydrate and total and saturated fat in the LFHC and VHFLC groups were 51% and 11% of energy, 29% and 71% of energy, and 12% and 34% of energy, respectively, with no difference in protein and polyunsaturated fatty acids. Mean energy intake decreased by 22% and 14% in the LFHC and VHFLC groups. The diets similarly reduced waist circumference (11-13 cm), abdominal subcutaneous fat mass (1650-1850 cm3), visceral fat mass (1350-1650 cm3), and total body weight (11-12 kg).

Different people respond differently to specified food. Cell Metabolism, 2017

We found no significant differential effects of bread type on multiple clinical parameters. The gut microbiota composition remained person specific throughout this trial and was generally resilient to the intervention. We demonstrate statistically significant interpersonal variability in the glycemic response to different bread types, suggesting that the lack of phenotypic difference between the bread types stems from a person-specific effect

Mindfulness eating seems to be effective addressing bad eating habits. frontiers in Psychology, 2018

In this article, we have provided the theoretical framework and early empirical evidence for an intervention that meets these criteria. Mindful awareness of habitual, maladaptive eating behaviors may help people to improve their relationships with food. When people have a clear window through which to view how habit loops are developed (e.g., eating when stressed) and maintained (e.g., reward-based learning), engaging in interventions that directly disrupt these loops (such as the mindful eating program we have described) can be an empowering process. That is, honing interventions to directly focus on core elements of the habit loop, rather than developing behavioral workarounds, may affect more lasting change.

Saturated fat's seems not bad, but trans fats are. BMJ, 2015

Saturated fat intake was not associated with all cause mortality (relative risk 0.99, 95% confidence interval 0.91 to 1.09), CVD mortality (0.97, 0.84 to 1.12), total CHD (1.06, 0.95 to 1.17), ischemic stroke (1.02, 0.90 to 1.15), or type 2 diabetes (0.95, 0.88 to 1.03). Total trans fat intake was associated with all cause mortality (1.34, 1.16 to 1.56), CHD mortality (1.28, 1.09 to 1.50), and total CHD (1.21, 1.10 to 1.33) but not ischemic stroke (1.07, 0.88 to 1.28) or type 2 diabetes (1.10, 0.95 to 1.27). 

Meals with low glycemic response shift metabolism to fat oxidation over carbohydrates. Journal of Clinical & Translational Endocrinology, 2016

After LGI meals in the whole body calorimetre, iAUC for glucose (P = 0.008) was lower compared to the HGI session. The HGI treatment produced a significantly greater MAGE than the LGI treatment over the 24 hour period (P < 0.001). Additionally, higher fat oxidation and lower carbohydrate oxidation were observed following breakfast and lunch when comparing LGI to HGI (P < 0.05)

Adding fat into meal may slow down glycemic response The British Journal of Nutrition, 1989

Addition of fat to either component of the meal reduced postprandial blood glucose (P less than 0.05) and insulin responses, but when the fat was incorporated in the soup, peak glucose and insulin responses were delayed as well (P less than 0.05). 6. The results show that the effect of fat on gastric emptying and absorption of nutrients depends on when, in relation to the other components of the meal, the fat is consumed.

Intermittent fasting may have beneficial effect on obesity and fat tissue (mice) Cell Metabolism, 2018

Here, we show that an every-other-day fasting (EODF) regimen selectively stimulates beige fat development within white adipose tissue and dramatically ameliorates obesity, insulin resistance, and hepatic steatosis. EODF treatment results in a shift in the gut microbiota composition leading to elevation of the fermentation products acetate and lactate and to the selective upregulation of monocarboxylate transporter 1 expression in beige cells.

Fasting-mimicking diet reduce intestinal inflammatory, improve immunity biomarkers and microbiota, reduce IBD, but human RCT is required Cell Reports, 2016

These results suggest that FMD cycles can reduce systemic inflammation and the associated increase in lymphocyte counts or percentage in both mice and humans. A randomized clinical trial on IBD patients is necessary to test the hypothesis that FMD cycles reduce IBD pathology in humans.

Fasting-mimicking diet composition Cell Press, 2019

Vegetable Soup: Rice Flour, Dried Onion, Inulin (Chicory Fiber), Dried Tomato, Dried Carrot, Salt, Dried Red Pepper, Dried Leek, Potato Starch, Olive Oil, Freeze-dried Basil, Spinach Powder, Dried Parsley, Natural Flavor.
Mushroom Soup: Rice Flour, Carrot Powder, Dried Onion, Champignon Mushroom Powder, Inulin (Chicory Fiber), Dried Champignon Mushroom, Salt, Yeast Extract, Potato Starch, Olive Oil, Dried Parsley, Natural Flavor.
Tomato Soup: Rice Flour, Dried Tomato Powder, Dried Onion, Inulin (Chicory Fiber), Potato Starch, Dried Tomato Pieces, Olive Oil, Salt, Yeast Extract, Dried Basil, Dried Parsley, Natural Flavor. Energy Drink Mix: Purified Water, Natural Vegetable Glycerin, Polylysine (Natural Preservative).
Energy Bar: Almond Meal, Macadamia Nut Butter, Honey, Pecan, Coconut, Flaxseed Meal, Coconut Oil, Vanilla, Sea Salt.
Chip Snack: Kale, Red Bell Peppers, Cashews, Sunflower Seeds, Nutritional Yeast, Lemon Juice, Cayenne Pepper, Sea Salt.
Algal Oil: Gelatin, Glycerin, Purified Water, Turmeric (Color), Annatto Extract (Color).
Supplements: Vitamin A (as Beta Carotene), Vitamin C (Ascorbic Acid), Vitamin D (as Cholecalciferol), Vitamin E (as DL-Alpha Tocopherol Acetate), Vitamin K (as Phytonadione), Thiamine (as Thiamine Mononitrate), Riboflavin, Niacin (as Niacinamide), Vitamin B6 (as Pyridoxine HCI), Folic Acid, Vitamin B12 (as Cyanocobalamin), Biotin, Pantothenic Acid (as Calcium-D-Pantothenate), Calcium (as Calcium Carbonate and Tribasic Calcium Phosphate), Iron (as Ferrous Fumarate), Phosphorous (as Tribasic Calcium Phosphate), Iodine (as Potassium Iodine), Magnesium (as Magnesium Oxide), Zinc (Zinc Oxide), Selenium (as Sodium Selenate), Copper (as Cupric Sulfate), Manganese (as Manganese Sulfate), Chromium (as Chromium Picolinate), Molybdenum (as Sodium Molybdate). Proprietary Blend: Beet Root Powder, Spinach Leaf Powder, Tomato Fruit Powder, Carrot Root Powder, Collards Greens Powder, Collards (Kale) Leaf Powder. Other Ingredients: Stearic Acid, Microcrystalline Cellulose, Dicalcium Phosphate, Croscarmellose Sodium, Magnesium Stearate, Silicon Dioxide, Food-grade Shellac.


Recommendation for healthy people to restrict dietary cholesterol seems to be wrong.  Nutrients, 2018

The current literature does not support the notion that dietary cholesterol increases the risk of heart disease in a healthy individuals.


It seems there no reason to restrict salt intake in non-hypertensive healthy people. JAMA, 1998

These results do not support a general recommendation to reduce sodium intake. Reduced sodium intake may be used as a supplementary treatment in hypertension.


Omega-3 fatty acids didn't reduce All Cause Mortality, major CVD and cancer incidence. The New England journal of medicine, 2018

In the analysis of death from any cause (978 deaths overall), the hazard ratio was 1.02 (95% CI, 0.90 to 1.15). No excess risks of bleeding or other serious adverse events were observed. Conclusions: Supplementation with n-3 fatty acids did not result in a lower incidence of major cardiovascular events or cancer than placebo.


Coming soon!


Cognitive behavioral therapy seems to be working, at least in extreme sleep conditions Behavioral Sleep Medicine, 2019

The intervention consisted of one 60–70 min session of CBT-I and a self-management pamphlet. A consecutive series of 30 adult male offenders with acute insomnia from a UK prison completed measures of prospective sleep (daily sleep diary), insomnia symptoms severity (Insomnia Severity Index), and mood symptoms (Patient Health Questionnaire and General Anxiety Disorder) one week before and four weeks after receiving the intervention. Results: Pairwise t-tests revealed that a single shot of CBT-I was effective in reducing the severity of insomnia in adult male offenders (t = [29], 12.65, p < 0.001). Further, the results demonstrated moderate to large effect sizes for reductions in depressive (dRM = 0.77) and anxious (dRM = 0.83) symptoms, as well as insomnia severity (dRM = 2.35).

Earplugs and eyemask improve sleep in some conditions Journal of Sleep Research, 2018

Despite the heterogeneity of analysed studies and some common methodological issues (sample size, design, outcome parameters choice and comparison) earplugs and eye mask showed potential positive effects on sleep quality and the incidence of delirium in ICU patients.


Using antibiotics disrupts microbiome and lead to increased incidence of autoimmune diseases. The Lancet, 2017

Asthma incidence in children (aged 1–4 years) showed an absolute decrease of 7·1 new diagnoses per 1000 children, from 27·3 (26·8–28·3) per 1000 children to 20·2 (19·5–20·8) per 1000 children (a relative decrease of 26·0%). Reduction in incidence over the study period was associated with decreasing antibiotic use in infancy (age <1 year), from 1253·8 prescriptions (95% CI 1219·3–1288·9) per 1000 infants to 489·1 (467·6–511·2) per 1000 infants (Spearman's r=0·81; p<0·0001). Asthma incidence increased by 24% with each 10% increase in antibiotic prescribing

Microbiome of obese have increased capacity to harvest energy from food and transmissible through fecal transplantation. Obese microbiota had more Firmicutes compared with the lean microbiota (mice) Nature, 2006

We have used this model to provide direct experimental evidence that at least one type of obesity-associated gut microbiome has an increased capacity for energy harvest from the diet. 16S-rRNA-gene-sequence-based surveys confirmed that the ob/ob donor microbiota had a greater relative abundance of Firmicutes compared with the lean donor microbiota (Supplementary Fig. 4 and Supplementary Table 7). Furthermore, the ob/ob recipient microbiota had a significantly higher relative abundance of Firmicutes compared with the lean recipient microbiota

Microbiota metabolize L-carnitine, choline and phosphatidylcholine from meat to trimethylamine-N-oxide (TMAO) which may increase CVD and alter cholesterol metabolism, slowing it removal from blood and contribute to accumulation on artery walls. Nature, 2013

We demonstrate here that metabolism by intestinal microbiota of dietary L-carnitine, a trimethylamine abundant in red meat, also produces TMAO and accelerates atherosclerosis in mice. Omnivorous human subjects produced more TMAO than did vegans or vegetarians following ingestion of L-carnitine through a microbiota-dependent mechanism. Increased risks for both prevalent cardiovascular disease (CVD) and incident major adverse cardiac events (myocardial infarction, stroke or death), but only among subjects with concurrently high TMAO levels.

Obese human microbiota transplanted into mice cause obesity, lean human microbiota is not.  HHS, 2014

We transplanted fecal microbiota from adult female twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets representing different levels of saturated fat and fruit and vegetable consumption typical of the USA. Increased total body and fat mass, as well as obesity-associated metabolic phenotypes were transmissible with uncultured fecal communities, and with their corresponding fecal bacterial culture collections.

Artificial sweeteners (aspartame, sucralose, saccharin; stevia wasn't studied) alters gut microbiota and induce glucose intolerance. Antibiotics vanishes effect. Nature, 2014

We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. 

Obesity microbiome seems to persist after weight loss and result in weight regain. Antibiotics had vanished effect. Obese microbiome seems to lower flavonoid levels (apigenin and narigenin) which lead to reduced fat burn of adipocytes. Flavonoid supplementation vanishes effect. (mice)  Nature, 2016

Here we identify an intestinal microbiome signature that persists after successful dieting of obese mice and contributes to faster weight regain and metabolic aberrations upon re-exposure to obesity-promoting conditions. Faecal transfer experiments show that the accelerated weight regain phenotype can be transmitted to germ-free mice. Additionally, we find that the microbiome contributes to diminished post-dieting flavonoid levels and reduced energy expenditure, and demonstrate that flavonoid-based ‘post-biotic’ intervention ameliorates excessive secondary weight gain. 


Avoid using fluoroquinolones, it's seems it is safer to use amoxicillin and azithromycin Journal of the American College of Cardiology, 2019 

The adjusted RRs for current users of FQ compared with amoxicillin and azithromycin users were 2.40 (95% CI: 1.82 to 3.16) and 1.75 (95% CI: 1.34 to 2.29), respectively. The adjusted RRs for recent and past FQ users when compared with amoxicillin were 1.47 (95% CI: 1.03 to 2.09) and 1.06 (95% CI: 0.91 to 1.21), respectively.

Post-antibiotics prebiotics may impair indigenous microbiome recovery, but autologous fecal transplantation induce recovery  Cell, 2018

Compared to spontaneous post-antibiotic recovery, probiotics induced a markedly delayed and persistently incomplete indigenous stool/mucosal microbiome reconstitution and host transcriptome recovery toward homeostatic configuration, while aFMT induced a rapid and near-complete recovery within days of administration.

Glucose & Insulin

High blood glucose induce oxidative damage to vessels Cell Metabolism, 2013Journal of clinical investigation, 2001, European Health Journal, 2013

We show here that acute hyperglycemia in normal subjects causes an oxidative stress as evidenced by the raised circulating nitrotyrosine levels during the hyperglycemic clamp.
Overproduction of ROS by mitochondria is considered as a causal link between elevated glucose and the major biochemical pathways involved in the development of vascular complications of diabetes

Overproduction of ROS caused by high glucose leads to increased production of AGE (advanced glycation endproducts), activation of PKC (protein kinase C), vascular cell apoptosis and loss of cell survival signalling. High glucose may activate SHP-1 which inhibit survival of survival of pericytes (cells embedded within the walls of capillaries) in the retina and podocytes in the kidney (epithelial cells that cover the outer surfaces of glomerular capillaries). ER (Endoplasmatic Retuculum) stress as consiquence of increased protein synthesis in response to excess nutrients and high lipids level leads pancreatic β-cell failure Cell Metabolism, 2013

Overproduction of reactive oxygen species (ROS) as a result of altered glucose metabolism and formation of advanced glycation end-products (AGE) further amplifies this process by activating nuclear factor κB (NFκB) and other proinflammatory pathways.
Vascular cell apoptosis is caused by abnormal glucose metabolism, activation of protein kinase C (PKC), formation of AGE, increased production of ROS, release of proinflammatory cytokines from Müeller cells or microglia in the retina or from leukocytes adhering to capillary endothelium, loss of survival signaling stimulated by platelet-derived growth factor (PDGF) and other factors, and upregulation of angiostatic factors like Tie2
High glucose concentrations and diabetes can activate Src homology-2 domain-containing phosphatase-1 (SHP-1), a tyrosine phosphatase, in several tissues including the retina and renal glomeruli. This leads to the dephosphorylation and deactivation of specific growth factor receptors critical for survival of pericytes in the retina and podocytes in the kidney
Increases in protein synthesis, protein misfolding, or perturbations in Ca2+ and redox balance can disturb ER function, leading to the development of ER stress.ER stress has emerged as an important mechanism linking obesity and the development of insulin resistance. It is also involved in pancreatic β-cell failure due to chronic activation of this pathway in the hyperinsulinemic state associated with obesity and insulin resistance. Although the underlying mechanisms that cause ER stress in the context of obesity have only begun to be elucidated, likely causes include increases in protein synthesis in response to nutrient excess, elevated levels of lipids, and changes in ER calcium homeostasis

Increased plasma and intracellular (muscle) free fatty acids induce insulin resistance by inhibiting glucose transport and increase inflammation by dealing with TLR (Toll-Like Receptor, also lead inhibition of insulin receptor by JNK and induce Akt pathway) and NF-kB (which upregulate pro-inflammatory cytokines TNF-a and IL-6). Activating PPAR-γ lead to redistribution of fat from muscle and liver into adipocytes and improve insulin sensitivity  Journal of clinical investigation, 2000, Diabetes, 1997

These data suggest that increases in plasma fatty acid concentrations initially induce insulin resistance by inhibiting glucose transport or phosphorylation activity, and that the reduction in muscle glycogen synthesis and glucose oxidation follows.
lean insulin-resistant offspring of NIDDM parents showed 1) trimodal distribution of insulin sensitivity, 2) high fasting plasma FFA concentrations, 3) an inverse correlation between insulin sensitivity and FFA concentration, 4) low plasma gluconeogenic amino acid concentrations, and 5) defective insulin secretion when related to insulin sensitivity in the subgroup of very resistant offspring. These results suggest that, in this white population, insulin sensitivity may be determined by a single major gene and that alterations in FFA metabolism may play a role in the pathogenesis of NIDDM.
Hence, accumulation of intramuscular fatty acids (or fatty acid metabolites) appears to play an important role in the pathogenesis of insulin resistance seen in obese patients and patients with type 2 diabetes. Moreover, fatty acids seem to interfere with a very early step in insulin stimulation of GLUT4 transporter activity or hexokinase II activity.
activating PPAR-γ receptors in adipocytes and promoting adipocyte differentiation, these agents might promote a redistribution of fat from liver and muscle into the adipocytes
Free fatty acids bind Toll-like receptor (TLR) activating NF-kB through degradation of the inhibitory complex IkBα by IKKβ-kinase.
As a result, NF-kB triggers tissue inflammation due to up-regulation of inflammatory genes IL-6 and TNF-α.
Toll-like receptor activation by FFA leads to phosphorylation of insulin receptor substrate-1 (IRS-1) by c-Jun amino-terminal kinase (JNK) and PKC, thereby altering its ability to activate downstream targets PI3-kinase and Akt. These molecular events result in the down-regulation of the glucose transporter GLUT-4 and, hence, insulin resistance

Wrong science