Dr. Rhonda Patrick on the Joe Rogan Experience #901, fact-checked

What the evidence shows: The 86% figure comes from a real 2015 double-blind, randomized, placebo-controlled trial (Cipolla et al., Cancer Prevention Research) of 78 men with rising PSA after radical prostatectomy: 60 mg/day of stabilized sulforaphane for six months was associated with a PSA doubling time of 28.9 months versus 15.5 months on placebo, an 86% relative difference. That trial's pre-specified primary endpoint, a target reduction in the log-PSA slope, was not met; the doubling-time figure was a secondary outcome. A separate, smaller single-arm study using a different sulforaphane dose (200 micromoles/day in 20 men) found a more modest lengthening of PSA doubling time, from 6.1 to 9.6 months, with only one of eight responding participants seeing a substantial PSA decline. A 2023 systematic review of randomized trials of sulforaphane in cancer found roughly 75% of the studies at high risk of bias and concluded the evidence remains preliminary, calling for larger, more rigorous trials before clinical claims are made. The number Patrick cites is accurately drawn from a genuine clinical trial, but it describes a secondary endpoint in one moderate-sized study whose primary endpoint failed, not established proof that sulforaphane treats or reliably slows prostate cancer. (Patrick also states the treatment lasted about a month; the source trial's dosing period was six months.)

What the evidence shows: The claim references a 2014 randomized, placebo-controlled trial of 291 adults in Qidong, China, published in Cancer Prevention Research, which found that daily consumption of a broccoli-sprout beverage increased urinary excretion of a benzene metabolite (a mercapturic acid conjugate) by roughly 61% compared with placebo, an effect detectable beginning on day one and sustained through the 12-week intervention. A follow-up 2019 dose-response trial of 170 adults over 10 days corroborated the effect at full dose (+63.2%) but found no significant change at lower doses, indicating the response is dose-dependent. The 61% figure reflects a rise in a urinary biomarker indicating enhanced Phase II detoxification enzyme activity, not a direct measurement that 61% of the body's stored or circulating benzene was eliminated, and neither trial measured or demonstrated reduced cancer incidence or disease risk. The underlying randomized-trial finding on benzene-metabolite excretion is well-supported, but Patrick's phrasing risks being read as a claim about literal benzene clearance from the body rather than a biomarker shift.

What the evidence shows: Patrick states that roughly 40% of patients respond to standard antidepressants versus about 30% on placebo. Published analyses of FDA-trial data support figures in this range: a 2015 World Psychiatry review of antidepressant efficacy found that the magnitude of symptom reduction across FDA trials was about 40% with antidepressants and about 30% with placebo, and separately noted that the NIMH-funded STAR*D study found citalopram produced a therapeutic response in only about 4 of 10 depressed outpatients. The NIMH's own summary of STAR*D reports that at the first treatment level, about one-third of participants achieved remission and another 10-15% responded without remission, consistent with an overall response rate in roughly the 40-48% range. Exact figures vary depending on the specific trial, drug, symptom scale, and whether response or remission is measured, but Patrick's 40%-versus-30% framing falls within the range reported in this peer-reviewed literature on antidepressant and placebo response rates. The claim is a reasonably accurate, if simplified, paraphrase of published data rather than a misstatement.

What the evidence shows: Patrick's specific factual claim, that a human clinical trial showed nicotinamide riboside (NR) to be safe and to raise blood NAD+ levels at doses as low as 100 mg/day, matches the peer-reviewed literature available at the time. Trammell et al. (2016, Nature Communications) reported the first controlled human pharmacokinetic trial of NR, giving healthy adults single oral doses of 100, 300, and 1,000 mg; all doses, including 100 mg, produced a measurable, dose-dependent rise in the blood NAD+ metabolome, and no serious adverse events occurred across 36 days of observation. A University of Iowa press release on the same study likewise states NR "safely boosts human NAD+ metabolism" with no serious side effects at any dose tested. This narrow safety/biomarker claim is well-supported; it is separate from, and should not be conflated with, the extensive mouse anti-aging and disease-reversal findings Patrick discusses elsewhere in the same segment, since no human trial existing at the time of this 2016-era study had demonstrated equivalent functional anti-aging or disease outcomes in people.

What the evidence shows: The claim references a 2016 analysis of the Women's Healthy Eating and Living (WHEL) cohort study (Marinac et al., JAMA Oncology), which followed 2,413 women with early-stage breast cancer and found that fasting fewer than 13 hours per night was associated with a 36% higher hazard of breast cancer recurrence compared with fasting 13 or more hours (hazard ratio 1.36; 95% CI, 1.05-1.76). Patrick's rounded "40%" figure is a reasonably close paraphrase of that 36% figure, but the framing as women who fast longer "reduce their recurrence risk" implies a causal, protective effect that this observational, self-reported dietary data cannot establish; the study's own authors called it an exploratory, hypothesis-generating analysis, noted they did not adjust for multiple comparisons, and stated randomized trials are needed to test causality. No association was found between nightly fasting duration and breast cancer-specific mortality in the same cohort. A 2023 systematic review of intermittent fasting and breast cancer found this finding has not been replicated in other studies and concluded evidence for fasting reducing recurrence in humans remains weak and insufficient. The underlying statistic is approximately accurate, but the causal, actionable framing overstates what a single observational cohort analysis supports.

What the evidence shows: A 2016 JAMA Internal Medicine historical analysis of internal Sugar Research Foundation (SRF) documents by Kearns, Schmidt, and Glantz found that the SRF paid $6,500 (about $48,900 in 2016 dollars) to three Harvard School of Public Health researchers, D. Mark Hegsted, Robert McGandy, and department chair Fredrick Stare, to produce a literature review on sugar, fat, and coronary heart disease. That review was published as a two-part article in the New England Journal of Medicine in 1967 and concluded that reducing dietary cholesterol and replacing saturated fat with polyunsaturated fat was the key dietary change needed to prevent heart disease, while downplaying evidence implicating sucrose. The SRF's funding and role in shaping the review were not disclosed at the time; NEJM did not require such disclosures until 1984. Patrick's figures and framing closely track the documented record: three Harvard scientists, a 1967 NEJM review, and a period-adjusted payment ($48,000-$49,000) in the same range as her stated $50,000. The claim is well-supported by the peer-reviewed historical analysis and contemporaneous reporting.