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Sugar-sweetened beverages have long been implicated in weight gain and nutrition-related diseases such as diabetes. But the effects of liquid sugar extend to longevity, as well. In fact, consumption of sugar-sweetened beverages is associated with dramatically accelerated telomere shortening – equivalent to as much as five years of a person's life. In this clip, Dr. Elissa Epel discusses the harmful effects of what she calls a "toxic lifestyle," one that includes the consumption of sugary drinks.
Rhonda: Back to the sugar-sweetened beverages you mentioned because I did read that study, your study that was on the sugar-sweetened beverages and how that was associated with accelerated telomere shortening by something like close to five years or something. I think if I remember correctly it was something like that. Where people that were drinking, you know, a lot of these sodas and sugar-sweetened beverages had their biological age as marked by a telomere length looked older than their actual chronological age. And so that was quite disturbing.
Elissa: Right. You know, that sugared beverage finding has been replicated many times by now. And it's not surprising because liquid sugar has been more of an effect than sugar in food. It does cause, you know, a big metabolic disturbance immediately. And so if you're drinking that every day, you should expect to have...across the spectrum of aging biomarkers to have them be accelerated. And so, you know, it's coming out to be one of the biggest predictors of obesity and diabetes, which...I'm talking about processed sugar, not just calories, particularly liquid sugar.
So, you know, we can all do our best to not have it. But what's even more powerful is when we get rid of it in our environment. So we just completed a study at our university where we just... this university banned all sugary beverages. It's because... I mean, it's just so ridiculous.
Rhonda: That's awesome.
Elissa: Yeah, it's awesome, it's amazing.
Rhonda: Go UCSF.
Elissa: I mean, it's so ironic that you go into, you know, many hospital cafeterias and that's the drink that they're selling and you know... so bottom line is that it reduced drinking dramatically, and it reduced waist size just getting rid of it at work. People could still have it at home, they can still bring it to work. So those are kind of things...
Rhonda: Limiting the access.
Elissa: We have to think about. Like you know, your child's eventual school and these environments that you want to keep children who are still developing habits surrounded by the healthy choices.
Rhonda: Right. I remember reading... and this was an animal study where should these sugar-sweetened beverages activated dopamine pathways and like a reward pathway in the brain. Similar to like some very bad recreational drugs. I mean, not the same...it wasn't as robust but like Methamphetamine. I mean these things. And I mean, you know, that is definitely I would say pretty scary that there's an addictive aspect to the sugar as well.
Elissa: Well, I mean, I think that cannot be understated about why that is an epidemic that we cannot control yet. So in health span, we're doing okay preventing people from dying from diseases, right, because we have medications and diagnostics. And so heart disease, stroke, like people are dying less from those, we're doing so well at keeping people alive and reducing those diseases. But at the same time, while those incidents and deaths are going down, the obesity incidence is going up. We cannot control it, we don't have a medication for it, and it's addictive.
Rhonda: And I think you just brought up a really good point. I mean, if medication is doing one thing where it's sort of like maybe extending a couple of years of your life because you're not gonna have a heart attack or stroke as soon but you're not fixing the problem, the cause of the problem which could be your unhealthy diet or a variety of other types of psychological stress or a combination of them lack asleep.
So it is really important to address, you know, the problem, what's causing you to, you know, be at a higher risk for type two diabetes or cardiovascular disease, or stroke, and address that problem. Because where a medication may help give you a couple more years, the quality isn't gonna be improved ...
Elissa: That's right.
Rhonda: ...if you don't fix it.
Elissa: That's right and quality is what matters. And then if you're having a toxic lifestyle, if you're sedentary and you're eating a junk food diet, that medication is not going to outweigh those big lifestyle effects. So like, let's take Metformin. Lots of people take Metformin for anti-aging, it's one of the very few pills that we have in sight that is probably slowing aging in some ways. But if you're taking Metformin and you're still eating a lot of sugar, like many people with diabetes are doing because they have...you know, their brain is wired that way right now with the hedonic addiction, that Metformin is doing very, very little. And so it's just an example of like, you know, let's work on these drugs, we absolutely need some breakthroughs to slow aging. But we cannot do it in this context of a toxic lifestyle.
A measurable substance in an organism that is indicative of some phenomenon such as disease, infection, or environmental exposure.
A neurotransmitter best known for its role in motor, motivation, and pleasure control. Dopamine also functions as a paracrine (cell-to-cell) hormone in other parts of the body. It is derived from tyrosine and is the precursor to norepinephrine and epinephrine. Some evidence suggests that dopamine may also be involved in pain modulation.
Relating to or characterized by pleasure. Hedonism is a school of thought that argues that pleasure and happiness are the primary or most important intrinsic goods and the aim of human life.
A drug commonly used for the treatment of type 2 diabetes. Metformin is in a class of antihyperglycemic drugs called biguanides. It works by decreasing gluconeogenesis in the liver, reducing the amount of sugar absorbed in the gut, and increasing insulin sensitivity. A growing body of evidence indicates that metformin modulates the aging processes to improve healthspan and extend lifespan. Furthermore, metformin may prevent genomic instability by scavenging reactive oxygen species, increasing the activities of antioxidant enzymes, inhibiting macrophage recruitment and inflammatory responses, and stimulating DNA damage responses and DNA repair.[1]
[1] Najafi, Masoud, et al. "Metformin: Prevention of genomic instability and cancer: A review." Mutation Research/Genetic Toxicology and Environmental Mutagenesis 827 (2018): 1-8.
A highly addictive psychostimulant drug. Methamphetamine, or “meth,” works by mimicking the actions of dopamine and serotonin, neurotransmitters produced in the brain that influence mood and movement. The drug produces an intense “rush” in users, followed by a hyperalert state. After it wears off, the brain is depleted of its dopamine, and depression is a common result. Methamphetamine appears to have neurotoxic (brain-damaging) effects, destroying brain cells that produce dopamine and serotonin.
An enzyme that extends the telomeres of chromosomes. Telomerase adds specific nucleotide sequences to the ends of existing chromosomes. Telomerase activity is highly regulated during development, and its activity is at an almost undetectable level of activity in fully developed cells. This lack of activity causes the cell to age. If telomerase is activated in a cell, the cell will continue to grow and divide, or become "immortal," which is important to both aging and cancer. Telomerase enzyme activity has been detected in more than 90 percent of human cancers.
Distinctive structures comprised of short, repetitive sequences of DNA located on the ends of chromosomes. Telomeres form a protective “cap” – a sort of disposable buffer that gradually shortens with age – that prevents chromosomes from losing genes or sticking to other chromosomes during cell division. When the telomeres on a cell’s chromosomes get too short, the chromosome reaches a “critical length,” and the cell stops dividing (senescence) or dies (apoptosis). Telomeres are replenished by the enzyme telomerase, a reverse transcriptase.
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