FoundMyFitness

This podcast features Jari Laukkanen, M.D., Ph.D., a cardiologist and scientist at the Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio. Dr. Laukkanen has been conducting long-term trials looking at the health effects of sauna use in a population of over 2,000 middle-aged men in Finland. The results? Massive reductions in mortality and memory disease in a dose-response fashion at 20-year follow-up.

In this almost 25-minute episode, we talk about...

• 00:00:37 - The association between sauna use and fatal cardiovascular outcomes.
• 00:00:37 - The inverse association between cardiovascular-related deaths and all-cause deaths.
• 00:02:00 - How men that used the sauna 2-3 times per week had a 27% lower cardiovascular-related mortality than men that used the sauna 1 time per week.
• 00:02:15 - How men that used the sauna 4-7 times per week had a 50% lower cardiovascular-related mortality than men that used the sauna one time per week.
• 00:02:50 - The confounding factors Dr. Laukkanen and his colleagues had to adjust for, such as physical exercise, cholesterol, obesity, smoking, alcohol consumption, socioeconomic status.
• 00:03:26 - The various types of cardiac-related deaths their reductions were shown in, including coronary artery disease, sudden cardiac death and more.
• 00:05:00 - How one of the major mechanisms by which sauna use improves heart health is by reducing blood pressure and incident hypertension.
• 00:05:40 - The mechanisms by which the sauna lowers blood pressure, which can occur via balancing of the autonomic nervous system, improvements in blood vessel function, decreases in arterial stiffness and compliance of arteries.
• 00:06:17 - The increases in heart rate seen with sauna use that make it similar to moderate aerobic exercise in some ways (up to 150 beats/min!).
• 00:06:56 - How time spent in the sauna was one of the more important factors for risk reduction with at least 20 minutes per session in a 174 F (79C) 4-7 times per week being a "sweet spot."
• 00:09:29 - The inverse, dose-response relationship between sauna use and all-cause mortality: 24% for 2-3 times per week, 40% for 4-7 times.
• 00:10:00 - His newest study that now shows a reduction in risk in a similar dose-response fashion for dementia and Alzheimer’s disease by around 65% for the most frequent sauna users.
• 00:10:18 - The way sauna use increases heat shock proteins which repair damaged proteins and prevent protein aggregates and how this could end up being at least one potential molecular mechanism at play.
• 00:13:03 - How sauna use increases growth hormone by 200-330%.
• 00:14:10 - The patterns of sauna use and especially whether to sauna before or after you weight train.
• 00:15:55 - The effect of sauna on mood which may be from improvements in cardiorespiratory fitness and possibly endorphins as well.
• 00:18:39 - How sauna improves heart rate variability.
• 00:20:04 - Cold-water immersion after sauna and a few cautionary words for extreme contrast therapy in people with a pre-existing heart condition that is currently unstable.

Send Dr. Jari Laukkanen a tweet on Twitter.

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Dr. Judith Campisi is a professor of biogerentology at the Buck Institute for Research on Aging and a co-editor in chief of the Aging Journal.

As an expert on cellular senescence, the discussion involves a lot of talk about aging and cancer, where senescence plays a very important fundamental role. What are some of the strategies we might use in the future to prevent senescent cells? What causes them in the first place?

In this 1-hour long conversation, we discuss a great number of very interesting things including:

• Why diseases of aging, despite occurring in vary diverse tissue types, all begin to crop up simultaneously after 50 or 60 years of life.
• What the fundamental molecular processes of aging are and what some of the on-going research and general thoughts are surrounding these processes.
• What senescence is and the evolutionary biology explanation for why we have the mechanism of cellular senescence in the first place.
• The infiltration of immune cells into our tissues that occurs as a function of aging and the role of damaged or senescent cells in attracting these immune cells.
• The changes in gut permeability that happens with age and how that may increase our susceptibility to chronic, low-level inflammation.
• The role of senescent cells in cancer metastasis and progression.
• The clearance of senescent cells as a valid life extension strategy.
• How mitochondrial dysfunction, even in the absence of DNA damage, can cause cells to undergo senescence.
• The interesting observation that senescence from damage versus energy crisis (failed mitochondria) demonstrates a different and unique phenotype of cellular senescence.
• The effects prolonged fasting may have on the clearance of senescent cells.
• How periodic prolonged fasts might mimic some of the effects associated with an mTOR dampening drug like rapamycin.
• How the secretions of senescent cells can affect the regenerative capacity of stem cells.
• The practicality of a consumer available clinical assays for DNA damage and the challenge of assessing tissue-specific senescence without the use of invasive biopsy.
• The effect of so-called fasting mimetic compounds (e.g. hydroxycitrate, resveratrol & spermidine) on senescent cells.
• And believe it or not much more!

Studies mentioned: 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17

Learn more about Dr. Judy Campisi.

Did you enjoy this podcast? It was brought to you by people like you!
Click here to visit our crowdsponsor page where you can learn more about how you can support the podcast for as little or as much as you like.

Dr. Gordon Lithgow of the Buck Institute for Research on Aging tells us about worms! Well, more accurately, his lab does research on nematodes, particularly an animal known as C. elegans.

This unassuming scientific model has a lot of important advantages for science: they can be frozen and subsequently thawed and retain viability, they are extremely well understood down to the precise number of cells in their body and the wiring of their nervous system, known as the connectome. Additionally, they have a short lifespan and are cheap to work with. Why would that be advantageous, you may ask?

This is where Dr. Lithgow's work on the Caenorhabditis Intervention Testing Program comes in. Short-lived organisms give Dr. Lithgow and his colleagues the opportunity to see how their biology responds to compounds in different contexts and to do so cheaply and rapidly. Think a vitamin, pharmaceutical or one of any number of other compounds may have a broad effect on longevity? Try it on Caenorhabditis first! Taking this approach allows the broad screening of compounds that might not otherwise get its chance in the limelight if science were limited to only working with rodents, for example.

But what could nematodes possibly have in common with us? The answer to the question is... gene homology! In fact, around 35% of C. elegans genes have a corresponding human version.

In this over 40-minute long conversation with professor Dr. Gordon Lithgow, we talk about...

• Nematodes... especially C. elegans, of course!
• The synergistic way in which research in lower organisms (C. elegans in this case) works together with rodent research to better understand the biology of aging and identify potential therapeutics.
• The story behind the Caenorhabditis Intervention Testing Program, a multi-institutional effort using the advantages of C. elegans short lifespan to screen for potential compounds that may increase lifespan. We also discuss the more expensive-but-closer-to-humans version of this program known just the Intervention Testing Program.
• The various qualities of C. elegans, especially as related to science's deep knowledge of the organism, that make it a perfect fit for this type of research.
• Some of the early experiences that actually lead to my early interest in the aging field and how it actually holds a bit in common with Gordon's story today.
• The role of protein aggregation as a possible fundamental mechanism of aging... even beyond its more established role in neurodegenerative diseases.
• Some of the fascinating research surrounding mild heat stress as a means to increase lifespan in lower organisms.
• Some of Gordon's research into the effects of metal accumulation, particularly iron, on aging in lower organisms and how, in humans, it may be important to approach the intake of these minerals with care.
• The interplay between genes that influence iron-binding and the development of Alzheimer's disease.
• Some of Gordon's research into the (perhaps surprising) effect of vitamin D on aging in C. elegans and, particularly, on the solubility of proteins... the loss of which is a feature of aging of particular interest.
• The critical involvement of the Nrf2 stress-response pathway in conferring benefits of vitamin D in worms... a pathway many of you may know about from previous discussions of sulforaphane, a robust activator of Nrf2 in humans.
• Some of the challenges encountered with ensuring standardization of protocols across all of the participating labs in the Caenorhabditis Intervention Testing Program.
• The amazing genetic diversity represented in soil-dwelling nematodes and how this is also an advantage in longevity research.
• The interesting possibility that certain compounds may have a different overall effect on lifespan or healthspan that is dependent within certain contexts (e.g. environmentally stressed or not).

Learn more about Dr. Gordon Lithgow.

Did you enjoy this podcast? It was brought to you by people like you!
Click here to visit our crowdsponsor page where you can learn more about how you can support the podcast for as little or as much as you like.

Have you done a 23andMe genetic test?
You can learn more about whether you have some of the specific polymorphisms discussed in this podcast, including ones related to the hemochromatosis and transferrin genes, by clicking here.

If you're anything like me, having the facts straight can sometimes help you to push through the tough part of building new habits or breaking old bad ones. This podcast talks about the realities about what the science says surrounding the consumption of refined sugar.

Some of the facts may surprise you! We talk about the relationship of consumption of refined sugar with...

• mortality and aging
• brain function, memory, and neuroinflammation
• the development of cancer and expression of oncogenes
• sex hormones

... and, of special relevance, if you're hoping to cut out a soda habit, the real addictive properties of refined sugar consumption that mirror that of more well-known drugs of abuse.

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Studies mentioned in podcast:
1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 10, 11, 14, 15, 16, 17, 18, 19

Today we try to answer or at least explore a big question in the world of health: does saturated fat cause heart disease?

This is not an unreasonable concern given the fact that there have been several associative studies that have found a link between saturated fat and heart disease, which is, no doubt, a fat that we find abundantly in the typical American diet since it is richly found in staples like fatty beef, pork, butter, cheese, and other dairy products.

And if you're in the United States and you're not at least a little concerned about heart disease, you may be asleep at the wheel since it's currently our leading cause of death.

Studies mentioned in this episode:

• Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis.
• Visceral adiposity and metabolic syndrome after very high–fat and low-fat isocaloric diets: a randomized controlled trial.
• Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial.
• Personalized Nutrition by Prediction of Glycemic Responses.
• Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease.
• Added sugar intake and cardiovascular diseases mortality among US adults.

Genetics resources:

• 23andme.com
• promethease.com
• foundmyfitness.com/genetics

Does meat consumption cause cancer? Or, put another way… does avoiding meat help prevent cancer?

If you aren't already savvy to the topic, this may sound more absurd than it should. Here's why: there have been many, many, many correlative studies that have found that higher meat consumption is associated with a significantly higher risk of cancer and cancer mortality.

To try to answer this question we end up going deep into discussing plausible mechanisms that might help explain this phenomenon and, indeed, discussing a little bit of cancer biology as well.

Some of the publications mentioned in this podcast:

• Association of Animal and Plant Protein Intake With All-Cause and Cause-Specific Mortality
• Effect of aerobic exercise on insulin, insulin-like growth factor-1 and insulin-like growth factor binding protein-3 in overweight and obese postmenopausal women
• Prospective study of colorectal cancer risk in men and plasma levels of insulin-like growth factor (IGF)-I and IGF-binding protein-3
• Polymorphic variants of insulin-like growth factor I (IGF-I) receptor and phosphoinositide 3-kinase genes affect IGF-I plasma levels and human longevity: cues for an evolutionarily conserved mechanism of life span control.
• Functionally significant insulin-like growth factor I receptor mutations in centenarians
• Congenital IGF1 deficiency tends to confer protection against post-natal development of malignancies
• Changes in plasma somatomedin-C in response to ingestion of diets with variable protein and energy content

The World Health Organization estimates that more than 350 million individuals of all ages have depression and approximately one-third of all patients with depression fail to respond to conventional antidepressant therapies like SSRI’s.

The good news is that today, perhaps more than ever, good science is starting to illuminate some of the underlying biological mechanisms surrounding the development of depression. This new understanding may soon help the clinical world develop new approaches to treatment that may be vastly more effective and for a greater number of people than the traditional approaches.

Publications mentioned:

• Antidepressants versus placebo in major depression: an overview

• Inflammation: Depression Fans the Flames and Feasts on the Heat

• Association of high-sensitivity C-reactive protein with de novo major depression.

• Sex Differences in Depressive and Socioemotional Responses to an Inflammatory Challenge: Implications for Sex Differences in Depression

• Dopaminergic Mechanisms of Reduced Basal Ganglia Responses to Hedonic Reward During Interferon Alfa Administration

• Inflammation-induced anhedonia: endotoxin reduces ventral striatum responses to reward.

• Structural and functional features of central nervous system lymphatic vessels

• Endurance exercise increases skeletal muscle kynurenine aminotransferases and plasma kynurenic acid in humans

• Psychological stress and corticotropin-releasing hormone increase intestinal permeability in humans by a mast cell-dependent mechanism

• Neurobiology: Rise of resilience

• First biological marker for major depression could enable better diagnosis, treatment

• Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial

• Sweetened-Beverages, Coffee, and Tea in Relation to Depression among Older US Adults (P05.122)

• Consuming highly refined carbohydrates increases risk of depression

Dr. Roland R. Griffiths is a clinical pharmacologist at Johns Hopkins and has been researching mood-altering compounds for over 40 years. As an unusually prolific scientist, having published over 360-times, he's also responsible for having started the psilocybin research program at Johns Hopkins nearly 2 decades ago.

In this 1-hour and 15-minute podcast, we discuss…

• 00:01:03 - the broader story of Dr. Griffiths 40 years of mood-altering drug research, including what got him started and how taking up a meditation practice ultimately influenced the eventual focuses of his research.
• 00:02:22 - the effect psilocybin has had in clinical trials in eliciting so-called mystical experiences that can act as a long-term catalyst for meaningful spiritual change and is amenable to being reproduced and clinically studied in a prospective manner.
• 00:03:45 - what distinguishes psilocybin from other drugs, particularly when reflecting backward on the experience months afterward.
• 00:05:11 - the process by which Dr. Griffiths and his team create an appropriate “setting” and facilitate feelings of safety for those participating in his trials.
• 00:06:42 - the elusive fundamental nature of a classical psychedelic experience whereby people often simultaneously describe the experience as ineffable (indescribable) but yet also often assign it a truth value that may even exceed that of everyday consensus reality.
• 00:07:36 - a description of the core features of a classical mystical experience that overlap with those found in a mystical experience induced by psilocybin.
• 00:08:58 - the qualities of the experience that Dr. Griffiths believes to most underlie the “reorganizational” potential it can have.
• 00:10:55 - the interesting potential areas for scientific exploration that the reproducibility of the psilocybin experience makes the substance amenable to.
• 00:11:25 - the promise psilocybin has shown as an effective therapeutic for anxiety and depression in patients with life-threatening cancer and also treatment-resistant depression in otherwise healthy patients (00:18:46).
• 00:13:04 - the lack of rigor in the very early trials on these compounds and the way in which cultural stigma surrounding psychedelic drugs ultimately played a role in impeding real, substantive clinical research for decades afterward.
• 00:16:31 - the long-term resilience of the antidepressant and anxiolytic effect, lasting six months and possibly even longer.
• 00:21:01 - the effect psilocybin has demonstrated in animal studies to increase hippocampal neurogenesis and enhance extinction of trace fear conditioning.
• 00:23:07 - the somewhat unintuitive neurobiological mechanism that may tie together some of the antidepressant properties of both psilocybin and ketamine, an anesthetic currently being studied as a rapid-onset antidepressant.
• 00:25:16 - whether or not the mystical subjective experiences are necessary for drugs like psilocybin to exert their antidepressant or anxiolytic effects.
• 00:26:43 - what the default mode network is and what its pattern of activity is in depression, long-term meditators, and after the acute use of psilocybin.
• 00:32:16 - the hard problem of consciousness.
• 00:37:26 - the challenge of finding the neurological correlates to match the phenomenology of individual’s subjective experiences.
• 00:38:16 - the promise psilocybin has shown in a small trial on smoking cessation where 60% of the treatment group were still abstinent a year afterward and plans Dr. Griffiths has to expand this area of research
• 00:41:10 - the possibility that the “reorganizational nature” of these experiences may open up new avenues as trials continue to try to embed the experience within different therapeutic contexts.
• 00:44:02 - the roadmap to FDA approval for use of psilocybin as a medication, particularly in the context of cancer-associated depression and anxiety.
• 00:45:05 - the risks inherent in taking psilocybin and the frequency of self-reported negative experiences in the general population.
• 00:47:22 - the criteria Dr. Griffiths and his colleagues use when screening for volunteers to participate in his studies involving psilocybin.
• 00:49:21 - the inability for clinicians to predict who is at risk of having challenging experiences defined by fear and anxiety (“bad trip”) and whether or not it is desirable, in terms of achieving a therapeutic outcome, to prevent these types of experiences altogether or not.
• 00:51:43 - the sort of dosages used in the trials.
• 00:54:45 - the clever ways devised by Dr. Griffiths to placebo control trials where expectation itself can affect outcome.
• 00:57:45 - some of the interesting anecdotes gleaned from Dr. Griffiths’ working with long-term meditators participating in the psilocybin trial.
• 01:05:13 - a brief discussion about some of the other psychedelics besides psilocybin, such as salvia divinorum and DMT (at 01:10:24).
• 01:12:08 - the historical indigenous use of psychedelics in various cultures spread throughout the world.

Watch this as a video on YouTube.

Dr. Jed Fahey is a multi-decade veteran of isothiocyanate research and is the director of the Cullman Chemoprotection Center at Johns Hopkins University.

Much of this conversation, as you might expect given Dr. Fahey's pedigree as a research scientist, is focused on isothiocyanates and, indeed, sulforaphane!

While we covered quite a lot on this very topic (isothiocyanates) via my solo podcast a few weeks ago, this covers everything that may have been overlooked.... and, indeed, so much more! Skip to the timeline below for a sampling.

Dr. Fahey and his colleagues have been, in a big way, at the absolute center of what is a staggering amount of research on these very powerful compounds.

There is hardly a topic which we can discuss in which he doesn't have an anecdote about a study he was involved in, or, in some cases, tribal knowledge that may not even be published but is nonetheless interesting and an important part of the story that is unique to his particular vantage point.

In this 2-hour and 30-minute interview, we discuss...

• 00:00:00 - the early history of sulforaphane research, including key initial discoveries.
• 00:00:37 - the serendipitous unfolding of events that lead to the converging of the research on the NRF2 stress response pathway with the sulforaphane-related research going on at the same institute Johns Hopkins.
• 00:05:06 - why cruciferous vegetables bother to create isothiocyanates in the first place.
• 00:07:26 - the involvement of the heat shock proteins, in addition to the increased activity of Nrf2, as an additional cellular response mechanism that's been observed in association with sulforaphane.
• 00:08:11 - how sulforaphane affects a diverse array of biochemical processes from glutathione synthesis to elimination of reactive oxygen species and detoxification of harmful compounds, including carcinogens.
• 00:15:01 - whether or not to cook your cruciferous vegetables.
• 00:15:34 - the epidemiological (associative) evidence that cruciferous vegetable consumption may help reduce the risk of cancer.
• 00:18:30 - the extremely unpredictable nature of endogenous conversion of glucorapahanin (the precursor) into sulforaphane between person to person.
• 00:22:14 - practical information surrounding supplementation of sulforaphane.
• 00:27:05 - the effect one particular french sulforaphane supplement had on the doubling rate of PSA, which is a marker for prostate cancer recurrence in prostate cancer patients.
• 00:28:17 - the role that the Cullman Chemoprotection Center at Johns Hopkins has played, in addition to fundamental research, in providing early, vital infrastructure enabling some of the efforts of the international research community in elucidating the effects of sulforaphane and related compounds and the underlying biological pathways.
• 00:28:26 - the incredible, almost geometric growth in new studies that has occurred since the advent of a few of the key discoveries about sulforaphane and its method of action.
• 00:32:48 - the practicality of probiotics as a way to improve endogenous myrosinase activity needed to convert the precursor to sulforaphane into the bioactive sulforaphane.
• 00:33:26 - the involvement of our gut bacteria in our ability to convert the precursor of sulforaphane into its active form.
• 00:37:13 - whether or not endogenous myrosinase activity improves as a function of repeated challenge with glucoraphanin (the precursor to sulforaphane).
• 00:39:30 - why probiotics may vary in their degree of efficacy.
• 00:43:00 - why consuming isothiocyanates to reduce the number of bacterial colonies of h. pylori, a risk factor for peptic ulcers and stomach cancer, may turn out to be a better intervention than complete eradication of the species with antibiotics.
• 00:47:21 - the bizarre relationship h. pylori has with childhood asthma, where it has been shown that having some h. pylori seems to reduce asthma incidence in childhood.
• 00:52:28 - the effect sulforaphane has on inflammation and why inflammation is often a great therapeutic target for many different diseases, including diseases of aging.
• 00:54:05 - the life extension properties broccoli has been shown to have in an insect model of aging.
• 00:59:27 - the underlying causes of Hutchinson-Gilford progeria and the promise sulforaphane may hold for this disease of rapid aging.
• 01:09:00 - the effects of sulforaphane or Nrf2 activation on diseases of the brain, such as autism (human evidence) and Alzheimer's (animal evidence), possibly through anti-oxidative or anti-inflammatory effects.
• 01:11:09 - the so-called autistic fever response whereby autistic patients report a sudden reversal of symptoms during brief periods of fever.
• 01:10:05 - the role heat shock proteins might play more broadly in the prevention of certain neurological diseases.
• 01:19:00 - the challenges inherent in clinical trials where scientists may be extremely optimistic about the effects that might be observed, but still have to exercise caution and choose trial conditions that may be conservative, for the good of the people whose lives and hopes hang in the balance.
• 01:27:01 - the role of inflammation and depression and what some studies on animals have demonstrated in terms of sulforaphane's potential as an antidepressant.
• 01:42:30 - a special isothiocyanate-containing plant known as Moringa or sometimes referred to as the drumstick tree or the horseradish tree.
• 01:46:32 - Dr. Fahey's inadvertent foray into the consumption of exotic meats during a visit to Africa.
• 01:51:15 - a compound commonly associated with broccoli: indole-3-carbinol and its downstream product diindolylmethane (DIIM).
• 01:57:00 - the practicality of using mustard seed powder as an extra source of myrosinase, possibly for your cooked cruciferous vegetables.
• 02:00:13 - whether or not it makes sense to freeze broccoli sprouts in order to extend their shelf life, and possibly even increase sulforaphane within certain contexts.
• 02:05:25 - Dr. Fahey's thoughts on where endogenous conversion of glucoraphanin occurs in the body, as well as how long it takes before sulforaphane metabolites hit the bloodstream after ingestion.
• 02:07:25 - Some general thoughts on frequency in terms of how often one might need to take sulforaphane to elicit its biological effects.
• 02:12:16 - why sulforaphane may one day be a component of sunscreen.
• 02:12:31 - what some of the upcoming trials involving sulforaphane are at the Cullman Chemoprotection Center.
• 02:17:07 - the incredible way in which a sulforaphane-rich broccoli sprout beverage was shown to dramatically enhance the detoxification of benzene through excretion: one study showed up to 61% starting immediately after supplementation.

You can find out more about Dr. Fahey and the Cullman Chemoprotection Center by visiting:

• The Cullman Chemoprotection Center Website (donation link)
• facebook.com/chemoprotectioncenter
• twitter.com/jedosan (Jed's twitter)
• jedfahey.com

This podcast is about one of the most important biological pathways you could possibly take the time to learn about: the NRF2 pathway.

The most potent naturally-occurring inducer of this pathway, a plant compound known as sulforaphane, may be one of the most potent health-enhancing compounds at our disposal and yet... no one is keeping it out of your hands! No $1,000 per pill markup is keeping it out of your hands -- it’s available to anyone willing to take the little bit of time it takes each week to produce broccoli sprouts.

In some respects, broccoli sprouts may even be a great equalizer in a way... while it’s true that healthy food can often be expensive, it’s even reasonably possible for a person to take $20 worth of seeds and feed their whole family some of the most healthful greens you could get your hands on. This video will tell you why.

Here are a few of the more salient points surrounding sulforaphane that are discussed in this podcast...

• Profound changes in lipid biomarkers, reducing heart disease risk by as much as 50% in humans.
• Massive reductions in cancer risk in humans and also highly effective as a cancer intervention, particularly prostate and breast but also many others.
• Steep reductions in inflammation in humans.
• Shown in mice to be as effective as prozac as an anti-depressant.
• Steep behavioral changes in humans with respect to certain neurological disorders, such as autism.
• Causes dramatic boosts in the excretion of air pollutants (up to 60%) in humans.

Key sections you may want to skip to:
00:03:35 - Cancer and mortality
00:21:56 - Aging
00:29:37 - Brain and behavior
00:41:33 - Final recap
00:44:18 - Dose

NOTE: If you enjoy this podcast, you'll enjoy the YouTube video more since it shows all of the figures and citations.