Type 2 diabetes can be reversed or put into remission within 30 days using lifestyle interventions.
"I managed to showcase to five million people in the UK each week that, you know, a condition like type 2 diabetes, for example—this is back in 2015—could be reversed, and I showed in 30 days that that reversal, or, you know, the technical term now here is to put it in remission, we could talk about that later." (said at 0:10:55)
Intensive dietary interventions (such as very-low-calorie diets or total diet replacement) can rapidly normalize fasting plasma glucose, liver fat, and beta-cell function within 1 to 4 weeks (30 days), allowing discontinuation of glucose-lowering medications in many individuals with early type 2 diabetes. However, according to international consensus definitions (including from the American Diabetes Association and Diabetes UK), formal clinical 'remission' requires maintaining non-diabetic glycemic levels (HbA1c < 6.5% / 48 mmol/mol) for at least 3 months in the absence of glucose-lowering medications. Thus, while acute glycemic normalization and reversal of underlying pathophysiologic defects occur within 30 days, establishing true clinical remission requires demonstration of sustained glycemic control over time.
- supports: Immediate and long-term effects of a very-low-calorie diet on diabetes remission and glyce… (Food science & nutrition 2019) · cited 43x in the literature
"Among 19 patients (age 48 ± 2 years, BMI 27.7 kg/m 2 ) who completed the study, rapid improvement in glycemic control was observed in the first 2 weeks of VLCD. At both 8 and 12 weeks, diabetes remission was achieved in 79%. Significant weight loss was accompanied by a significant reduction in IR and an increase in beta cell function, starting at 4 weeks of VLCD." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Very low calorie diets and total diet replacement in type 2 diabetes: where are we now? (Drug and therapeutics bulletin 2024) · cited 4x in the literature
"Management of type 2 diabetes has now been simplified by the understanding that the condition is caused by excess fat in the liver together with suppression of beta cell function by the associated excess liver export of fat. These factors can be reversed by substantial weight loss leading to remission in the early years after diagnosis, or at least major decrease in cardiovascular risks and improvement in glucose control for all. Weight loss by any means is successful, but it is most easily achieved by rapid action using a low or very low calorie diet of around 800 kcal/day followed by sustained modest restraint of dietary habits. Oral hypoglycaemic agents and one antihypertensive drug can be withdrawn on day 1 of the weight loss diet, raising the importance of appropriate deprescribing." (abstract, results, passage verified)
pubmedfull study (doi)
Chronic psychological stress causes increased intestinal permeability (leaky gut) and alters the gut microbiome composition.
"I explained to her how stress can alter the gut, it can, you know, having too much stress can absolutely cause holes to appear in our gut wall, you know, what we call leaky gut. We know that too much stress can alter the balance of gut bugs in our intestine, in our large intestine." (said at 0:19:19)
Preclinical and human experimental studies demonstrate that psychological stress activates the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system, prompting mast cell degranulation, modulation of epithelial tight junction proteins (such as claudins and occludin), and alterations in gut microbiota composition. However, stress does not cause physical or macroscopic "holes" in the intestinal wall; rather, it induces a microscopic increase in paracellular permeability across the epithelial barrier (often colloquially termed "leaky gut"). While animal models robustly show stress-induced intestinal hyperpermeability and dysbiosis, human evidence demonstrates more nuanced, modest, and transient increases in paracellular permeability.
- supports: Acute psychological stress increases paracellular permeability and modulates immune activi… (United European gastroenterology journal 2023) · cited 12x in the literature
"Dichotomous listening stress induced a subjective and objective stress response, and significantly increased paracellular but not transcellular permeability." (abstract, results, passage verified)
pubmedfull study (doi) - context: Psychosocial stress-induced intestinal permeability in healthy humans: What is the evidenc… (Neurobiology of stress 2023) · cited 43x in the literature
"In vitro and animal studies strongly suggest that psychosocial stress is one of the factors that can increase intestinal permeability via mast-cell dependent mechanisms. Remarkably, studies have not been able to yield unequivocal evidence that such relation between stress and intestinal permeability also exists in (healthy) humans." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Psychological stress and immune dysregulation: Insights from neuroimmunology and the gut-b… (Behavioural brain research 2026) · cited 2x in the literature
"Emerging research highlights the gut-brain-immune axis as a critical mediator of these effects, where alterations in gut microbiota composition, microbial metabolites, and intestinal barrier integrity modulate systemic inflammation, immune cell function, and neural activity." (abstract, results, passage verified)
pubmedfull study (doi)
Research demonstrates significantly higher circulating levels of LPS (lipopolysaccharide) in individuals with major depressive disorder compared to those without the condition.
"Well, that study was actually founded on previous research, supportive research, that demonstrated much higher levels of LPS—I'll explain in a moment—in major depressive disorder in comparison to those who do not." (said at 0:32:24)
While research linking bacterial translocation and gut permeability to depression demonstrates elevated immune responses to lipopolysaccharides (LPS)—specifically significantly higher levels of anti-endotoxin antibodies and soluble CD14 (sCD14) in depressed individuals compared to non-depressed controls—direct measurement of circulating LPS levels yields a more nuanced picture. Meta-analytic evidence shows clear elevations in immune markers triggered by bacterial endotoxins rather than consistent simple elevations of free LPS alone. Furthermore, clinical evaluations within major depressive disorder (MDD) cohorts have found that circulating LPS levels inversely correlate with depression severity and anhedonia, with severely depressed patients exhibiting lower circulating LPS concentrations than those with mild-to-moderate depression.
- context: Leaky Gut Biomarkers as Predictors of Depression and Suicidal Risk: A Systematic Review an… (Diagnostics (Basel, Switzerland) 2025) · cited 17x in the literature
"For depressive symptoms, when compared to the controls, patients showed significantly increased levels of intestinal fatty acid-binding protein (I-FABP) (ES = 0.36; 95% CI = 0.11 to 0.61; p = 0.004; I 2 = 71.61%), zonulin (ES = 0.69; 95% CI = 0.02 to 1.36; p = 0.044; I 2 = 92.12%), antibodies against bacterial endotoxins (ES = 0.75; 95% CI = 0.54 to 0.98; p < 0.001; I 2 = 0.00%), and sCD14 (ES = 0.11; 95% CI = 0.01 to 0.21; p = 0.038; I 2 = 10.28%). No significant differences were found between the patients and controls in levels of LPS-binding protein (LBP) and alpha-1 antitrypsin (A-1-AT)." (abstract, results, passage verified)
pubmedfull study (doi) - context: Higher Lipopolysaccharide Levels Are Linked to Less Anhedonia and Lower Severity of Major … (Brain sciences 2026)
"Patients with severe depression exhibited significantly lower circulating LPS levels than those with mild-to-moderate depression (95.6 vs. 165.2 pg/mL, p = 0.007), despite no significant differences in cytokine concentrations." (abstract, results, passage verified)
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