500mg of This Extract Stops Insulin Resistance AND Repairs Muscle — Transcript

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1. 0:00Two people can have the same amount of
2. 0:02muscle mass with radically different
3. 0:04mitochondrial health within that muscle
4. 0:06producing very different metabolic and
5. 0:09functional outcomes. And there's a
6. 0:11compound that directly switches on the
7. 0:13recycling system inside your muscle
8. 0:15cells. The same system that fails as you
9. 0:17age and drives muscle loss from the
10. 0:19inside out, especially if you have the
11. 0:22lower mitochondrial content muscle,
12. 0:24which you would never really know
13. 0:25looking at you from the outside. The
14. 0:27clinical data is showing this compound
15. 0:28doesn't just improve muscular strength,
16. 0:30muscular endurance, but it also drops
17. 0:32key markers that are tied to insulin
18. 0:34resistance. But the big problem with
19. 0:36this compound is that 88% of people have
20. 0:39zero detectable levels of it in their
21. 0:41blood. It's not because they can't
22. 0:42produce it or they're not utilizing it
23. 0:45properly, but it's because one specific
24. 0:47condition isn't being met. The good news
25. 0:48is that that's fixable and I'm going to
26. 0:50show you exactly how. So here's what
27. 0:51we're going to cover. First, we're going
28. 0:52to talk about why your muscles are
29. 0:54actually aging at the cellular level and
30. 0:56why it's not what most people would
31. 0:58think is happening. Then we'll talk
32. 0:59about a compound. It's actually a
33. 1:00pomegranate that can turn on your
34. 1:02muscles cleanup system and the clinical
35. 1:04trial that tested it. Then we're going
36. 1:06to talk about what I call the
37. 1:07pomegranate gap because you can eat
38. 1:08pomegranates, but 88% of people actually
39. 1:11miss out on this compound despite eating
40. 1:14the right stuff. Finally, I'm going to
41. 1:16talk about three different ways you can
42. 1:17get your levels of this compound up
43. 1:19through different pathways. So let's
44. 1:21start with what's actually happening
45. 1:22inside aging muscle. Most people would
46. 1:25look at muscle loss and they say it's
47. 1:26all about protein, it's all about
48. 1:27hormones. It could even be about
49. 1:29metabolic acidosis, that has an effect,
50. 1:31too. Like when your urea isn't really
51. 1:33being moved out of the body and your
52. 1:35acidosis goes up, that can matter. But
53. 1:37there was a review in the International
54. 1:38Journal of Biochemistry and Cell Biology
55. 1:41that laid out the case that
56. 1:42mitochondrial dysfunction is actually
57. 1:44the central driver of this. Your
58. 1:46mitochondria, which is the energy
59. 1:48production inside every muscle cell,
60. 1:51they accumulate DNA damage and this
61. 1:53happens over time because unlike your
62. 1:55regular DNA, mitochondrial DNA don't
63. 1:58have the ability to protect themselves.
64. 2:00So, they are much more susceptible to
65. 2:02damage and the damage builds and builds
66. 2:05and builds. And when that happens, your
67. 2:07mitochondria start fusing together into
68. 2:09these oversized networks that produce
69. 2:11more oxidative stress but less energy.
70. 2:13So, they become like through
71. 2:15mitochondrial fusion, your dysfunctional
72. 2:17mitochondria actually a bit more
73. 2:19powerfully dysfunctional. So, normally
74. 2:21your cells would clean those out through
75. 2:23a process called mitophagy and this is
76. 2:25basically tagging the broken
77. 2:27mitochondria and then recycling them.
78. 2:29Your body like goes around and it
79. 2:30labels, "Hey, you're busted. Hey, you're
80. 2:32messed up." It throws labels on
81. 2:33everything and then the body knows what
82. 2:35to do with them. But that cleanup system
83. 2:37itself degrades with age. So, you're in
84. 2:40a really tricky spot. So, this lysosome
85. 2:42part of the cell that really does the
86. 2:43recycling, it gets clogged up with a
87. 2:45particular compound. It's a toxic
88. 2:47buildup of it. So, now you've got
89. 2:49damaged mitochondria that can't be
90. 2:51cleared pumping out stress signals that
91. 2:53eventually trigger your muscle cells to
92. 2:55literally self-destruct. So, we get
93. 2:57atrophy. It's one of the main reasons we
94. 2:59lose muscle as we age. These aren't
95. 3:01abstract signals. The literature review
96. 3:04actually notes that mitochondrial
97. 3:05apoptotic signaling has been shown to
98. 3:08correlate directly with slower walking
99. 3:11speed and reduced muscle volume. So,
100. 3:14these are things that test this. They're
101. 3:16losing muscle mass, they're getting
102. 3:17weaker, their pep to their step is
103. 3:20literally going away. That is sarcopenia
104. 3:23at the literal cellular and functional
105. 3:25level. So, we're not just talking losing
106. 3:26muscle. It's more like your muscle cells
107. 3:29literally initiating their own death
108. 3:31because the recycling system has failed
109. 3:33it. And that tells you something super
110. 3:34important and that is that muscle
111. 3:36quality matters more than muscle
112. 3:38quantity. Quantity matters, too, but you
113. 3:40definitely want to have high quality and
114. 3:42quantity. So, two people can have the
115. 3:44same muscle mass but radically different
116. 3:45mitochondrial health within that muscle
117. 3:47producing very different functional
118. 3:48outcomes. So, the question becomes, can
119. 3:50we turn the recycling system back on?
120. 3:52And there's a compound I've talked about
121. 3:54before, it's called urolithin A. It's
122. 3:56extremely promising. It's what's called
123. 3:57a postbiotic. So, your gut bacteria
124. 3:59produce it when they break down specific
125. 4:01polyphenols that are called
126. 4:03ellagitannins. So, urolithin A directly
127. 4:06activates something called the PINK1 and
128. 4:09the Parkin pathway, which is the
129. 4:10molecular switch for this recycling
130. 4:12within the mitochondria for mitophagy.
131. 4:14Now, there's a randomized control trial
132. 4:15that was published in JAMA Network Open,
133. 4:17and it tested this in older adults. It
134. 4:19had 66 participants, half of them got
135. 4:211,000 mg of urolithin A daily, half got
136. 4:24a placebo, and they did this for 4
137. 4:25months. Now, the two primary endpoints
138. 4:28here, they looked at 6-minute walk
139. 4:29distance and maximal ATP production.
140. 4:32They did not reach statistical
141. 4:34significance, but the secondary endpoint
142. 4:36told a much more compelling story. Now,
143. 4:38however, those first endpoints still
144. 4:40showed a difference, just statistically
145. 4:42significant not as much. What they did
146. 4:44find is that urolithin A produced
147. 4:46significantly more muscle contractions
148. 4:49before fatigue in both the hand and the
149. 4:51leg in which they were measuring. So,
150. 4:53two completely different muscle groups
151. 4:55with different fiber compositions both
152. 4:56showing the same directional
153. 4:58improvement. That's exactly what you
154. 5:00predict if mitophagy is working better.
155. 5:02Endurance improves, strength improves,
156. 5:05because you've got healthier
157. 5:06mitochondria sustaining repeated
158. 5:08contractions. This is what preserves
159. 5:10your muscle, and this has an effect on
160. 5:12insulin resistance, because if your
161. 5:13muscle is functioning, you will absorb
162. 5:16more glucose. Let's just say this, you
163. 5:17have 100 lb of muscle, but you have
164. 5:19crummy mitochondria in that muscle, that
165. 5:21100 lb of muscle is very different for
166. 5:23someone that has 100 lb of muscle with
167. 5:25good functioning mitochondria, cuz
168. 5:26glucose is going to get utilized
169. 5:28properly and stored and burned. Hence,
170. 5:31the decrease in potential insulin
171. 5:32resistance. And the biomarkers back this
172. 5:34up, too. Acylcarnitines dropped. Those
173. 5:36are the intermediates that accumulate
174. 5:38when fat burning is not working well.
175. 5:40So, their reduction is one of the most
176. 5:41reliable blood markers that
177. 5:43mitochondrial function is genuinely
178. 5:45improving. They also saw that plasma
179. 5:47ceramides decreased, and inflammation,
180. 5:49CRP was lower. I mean, pomegranate is
181. 5:52the richest dietary source of
182. 5:53ellagitannins that you could possibly
183. 5:55eat. Okay, it gives you the precursors
184. 5:57that your gut bacteria need to make
185. 5:59urolithin A. So, you'd think that the
186. 6:01answer is just to eat more pomegranates,
187. 6:03and that definitely works, but it gets a
188. 6:04lot more nuanced than that. We're going
189. 6:06to get into the research behind that
190. 6:07because this is really important. And
191. 6:09again, I'll show you how you can get
192. 6:11your body to utilize it better. Now,
193. 6:12I'll also going to put a link down for a
194. 6:14product called Timeline Longevity. They
195. 6:17have a patented form of Urolithin A.
196. 6:19I've known them for a long time. They're
197. 6:21a Swiss company. I've worked with them.
198. 6:23I know the owner. Very good brand that
199. 6:26has actually published a lot of the
200. 6:27leading research on Urolithin A. So,
201. 6:29they are the real deal. And when you
202. 6:31have Urolithin A in a concentrated form,
203. 6:34you can utilize it. It's just hard to
204. 6:36extract it from food. There are ways you
205. 6:38can do it, and I really do recommend
206. 6:40that people get things from food
207. 6:41whenever possible. But, I also feel like
208. 6:43when you're looking at research,
209. 6:44Urolithin A is one of those compounds
210. 6:46that it does make sense in supplemental
211. 6:48form. It absolutely does. And the
212. 6:50evidence is just so strong there. So,
213. 6:52that link down below, that's for a 20%
214. 6:54off discount link. I'll put it in the
215. 6:55top line of the description. These guys
216. 6:57are the main ones. There's a lot of
217. 6:58fly-by-night companies that have started
218. 7:00to make Urolithin A. I'd even seen some
219. 7:02third-party research before that has
220. 7:03shown that like some of them don't even
221. 7:05have a They say they have It's not good.
222. 7:07Anyway, the link is down below for
223. 7:09Urolithin A. Check that out from
224. 7:10Timeline. Now, there was a study that
225. 7:12paints a picture interestingly. So, it
226. 7:14was in the European Journal Clinical
227. 7:16Nutrition. They took 100 people, and
228. 7:18they gave each person pomegranate juice
229. 7:20or a direct Urolithin A supplement.
230. 7:22Before any intervention, only 12% of
231. 7:25them had detectable Urolithin A in their
232. 7:26blood. So, 88% did not have Urolithin A.
233. 7:29And it's not because their bodies are
234. 7:30incapable. You have to have the right
235. 7:32bacterial conditions. It's like a
236. 7:35postbiotic. It has to be a perfect
237. 7:36storm. There's no way to really know.
238. 7:37So, after drinking a standardized
239. 7:39pomegranate juice, about 40% of them
240. 7:41reached meaningful levels, which means
241. 7:43that a good chunk of people do have the
242. 7:45machinery, but it just needs to have
243. 7:46like the right input. But, 60% still had
244. 7:49little or no Urolithin A. And what
245. 7:52researchers determined was that it was
246. 7:53the gut microbiome composition. So,
247. 7:55producers of Urolithin A had way greater
248. 7:58microbial diversity. Specifically, they
249. 8:00had more Akkermansia. They also had more
250. 8:02Ruminococcaceae families. So, very
251. 8:04specific bacteria. And these are species
252. 8:06that perform the conversion. Things
253. 8:08change a little bit when you look at the
254. 8:10rest of the research though. Okay, the
255. 8:12same participants that took 500 mg of
256. 8:14direct urolithin A, every single person
257. 8:17reached meaningful circulating levels.
258. 8:19So, the peak levels were sixfold higher
259. 8:21than pomegranate juice producers. The
260. 8:23microbiome bottleneck was bypassed. I
261. 8:26cannot ask someone to change their
262. 8:27microbiome composition. You can take all
263. 8:30the probiotics in the world, but your
264. 8:31lifestyle, your stress, your diet, it's
265. 8:33all going to determine what happens
266. 8:35there. So, even if you're one of the 40%
267. 8:37who can convert pomegranate, you're
268. 8:39probably not reaching the doses that we
269. 8:41can hit in these clinical trials. It
270. 8:42doesn't mean you're stuck though, cuz
271. 8:43there are multiple ways to close the
272. 8:45gap. Again, a urolithin A supplement, I
273. 8:47think is like the easiest low-hanging
274. 8:49fruit, but you know, it does cost some
275. 8:51money. There's some other things that we
276. 8:53have to look at. Like, mitophagy isn't a
277. 8:54single switch. There are multiple
278. 8:56independent pathways that activate it,
279. 8:58and you can stack them. So, there was a
280. 8:59review in Exercise and Sport Sciences,
281. 9:01and this established that exercise
282. 9:03triggers mitophagy through this AMPK
283. 9:05pathway, which is completely separate
284. 9:07from the PINK1 Parkin pathway that
285. 9:09urolithin A uses. It's not the same, but
286. 9:12it's getting you some of the same
287. 9:13effect. So, when you exercise, ATP gets
288. 9:15consumed, and that creates an activation
289. 9:17of AMPK, which then activates ULK to
290. 9:20initiate the cleanup process. So, peak
291. 9:22mitophagy from exercise happened about 6
292. 9:25hours after the session. Now, this is
293. 9:27very direct because in this study, when
294. 9:29they knocked out ULK1, that pathway,
295. 9:32exercise-induced mitophagy was
296. 9:34completely blocked. Now, resistance
297. 9:36training, this has a big part, too. Very
298. 9:38relevant because mechanical loading
299. 9:40drives the fragmentation step, and this
300. 9:42is a precursor to the whole mitophagy
301. 9:43process. But in this case, intensity
302. 9:45matters. So, you have to lift heavy in
303. 9:48this case, and not everyone can do that.
304. 9:49And then there's the fasting piece.
305. 9:51There's a systematic review in the
306. 9:52Journal of Cachexia, Sarcopenia, and
307. 9:53Muscle, and it confirmed that caloric
308. 9:55restriction is one of the strongest
309. 9:57known genetic triggers for mitophagy.
310. 9:59And we know this, right, with autophagy.
311. 10:01But directly with the mitochondria, it's
312. 10:03interesting, too. So, fasting suppresses
313. 10:05mTOR, which is the main brakes on
314. 10:07autophagy, while simultaneously
315. 10:08activating AMPK and sirtuins. So, we see
316. 10:11in data that fasting directly
317. 10:13upregulates PINK1, parkin, NIX, and also
318. 10:16these other like LC3-II. These are
319. 10:18molecular markers of active autophagy
320. 10:20and mitophagy. So, we can get similar
321. 10:22effects to urolithin A with fasting,
322. 10:24particularly exercise during fasting.
323. 10:27But, urolithin A is working in a very
324. 10:29concentrated way down that PINK1
325. 10:31pathway. So, still stronger, but
326. 10:33combined with fasting, it's powerful.
327. 10:35The primary fasting pathway actually
328. 10:36runs through something called BNIP3 and
329. 10:39receptor-mediated signaling. This is
330. 10:41very distinct from the exercise pathway
331. 10:43and the urolithin A pathway. Okay, so
332. 10:45fasting does get you a unique benefit on
333. 10:48mitophagy. So, what do you actually do?
334. 10:50Okay, first off, pomegranate is
335. 10:51absolutely still worth eating.
336. 10:53Absolutely, because this is good stuff,
337. 10:55all right? The ellagitannins in
338. 10:57pomegranates feed the exact gut bacteria
339. 10:59that perform the conversion. So, if you
340. 11:01consistently consume pomegranates, you
341. 11:04do gradually shift your microbiome
342. 11:06towards a greater urolithin A
343. 11:08production, even if a single glass of
344. 11:10pomegranate juice does nothing today.
345. 11:12So, consistently, it will get better.
346. 11:14Now, it's not going to get you as high
347. 11:15as a direct urolithin A supplement,
348. 11:17which we get the huge benefit from, but
349. 11:19it will get better. The whole pearls are
350. 11:20in pomegranates are better to eat than
351. 11:22the juice because the fiber that is in
352. 11:24these little pearls specifically feeds
353. 11:26the good bacteria. Secondly, if you want
354. 11:27the clinically tested dose, you want to
355. 11:29supplement with urolithin A. Okay,
356. 11:31that's the reliable path that we've seen
357. 11:32in the literature. The trial used
358. 11:34between 500 and 1,000 mg daily. Third,
359. 11:36you want to stack your mitophagy
360. 11:38triggers. So, resistance training to
361. 11:40activate the AMPK pathway, a 14- to
362. 11:4216-hour overnight fast, and ideally
363. 11:44training at the end of that fast. Uh
364. 11:46also, if you're supplementing, consider
365. 11:48taking it with an evening meal so that
366. 11:50it's circulating during an overnight
367. 11:52fast. Okay, that way you're getting the
368. 11:53benefits of urolithin A happening during
369. 11:55your fast. So, all this, like three
370. 11:57distinct pathways, all running at once.
371. 11:59So, when we come back to 88%, like not
372. 12:02getting this stuff, that's truly it's
373. 12:04not a life sentence. It just means that
374. 12:06we're not really set up to get this
375. 12:07compound from food a lot. So, if you
376. 12:09consistently consume it, you'll get it.
377. 12:10You can change that. You just got to
378. 12:11build up the microbiome, you've got to
379. 12:13eat the right foods, you've got to do
380. 12:15the fasting. And I would recommend at
381. 12:17least occasionally taking your urolithin
382. 12:19A supplement, if not regularly. Now,
383. 12:21everything that we covered today is
384. 12:22about autophagy in the muscle, in the
385. 12:24mitochondria. But this same cleanup
386. 12:26process matters in your brain. So, I did
387. 12:27a full breakdown on how 5 g of glutamine
388. 12:30can actually double autophagy in the
389. 12:32brain and reduce neuroinflammation. So,
390. 12:35I'll link to that video right here. It's
391. 12:36a great next video to watch after
392. 12:38learning about this whole thing. And as
393. 12:40always, I'll see you