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Part 1 | Part 2 |PART 3| Part 4 | Part 5
Sugar:The Bitter Truth
Sugar:The Bitter Truth

40:12 So when you find a mistake, what do you do?
40:17 You admit the mistake and you right the ship.
40:21 We haven't admitted the mistake,
40:23 and we haven't righted the ship.
40:26 So, we've our food supply adulterated,
40:29 contaminated, poisoned, tainted.
40:32 On purpose, and we've allowed it, and we've let it,
40:37 thought the addition of fructose
40:38 for palatability, especially because of the decreased fat,
40:40 and also as a ostensibly browning agent,
40:44 which actually has it's own issues.
40:46 Because why it browns so well
40:48 with the sugar in it, actually is
40:49 what's going on in your arteries.
40:51 Because that's causing what we call
40:53 protein glycation and cross linking,
40:55 which is actually contribution to atherosclerosis.
40:57 So it works on your steak on the grill,
41:01 it works in your arteries the same way.
41:04 And removal of fiber also.
41:06 Now, why did we remove fiber from our diet?
41:09 We, as human beings walking the earth 50,000 years ago,
41:14 used to consume 100 to 300 grams of fiber per day.
41:18 We now consume 12.
41:21 Why? What did we do?
41:24 We took the fiber out.
41:26 So, why'd we take the fiber out?
41:29 It takes too long to cook,
41:30 takes too long to eat, and shelf life.
41:33 So, people ask me, "What's the definition of fast food."
41:36 Fiberless food.
41:38 I dare you, other than a salad, I dare you
41:40 to go to any fast food restaurant
41:42 and find anything on their menu
41:43 that they actually have to cook,
41:44 that has more than one gram of fiber in it.
41:47 'Cause there isn't any, and that's on purpose.
41:49 Because they take the fiber out,
41:50 'cause that way they can freeze it,
41:52 ship it around the world, and cook it up fast,
41:55 and not only is is fast cooking,
41:56 but it's fast eating, which also
41:58 causes it's own satiety issues.
41:59 Bottom line, we have a typhoon on our hands.
42:03 And then, finally, the last issue
42:05 was the substitution of transfats,
42:07 which are clearly a disaster,
42:08 but those have been going down,
42:10 because we know that those are a problem.
42:11 So we've actually gotten rid of most transfats,
42:14 not completely, but most.
42:16 So this is it, this is what we've done
42:18 over the last 30 years.
42:21 Now, to the biochemistry.
42:23 Now, how many of you here have taken biochemistry?
42:30 About 25%.
42:32 I am going to show you a lot of reactions
42:36 in excruciating detail.
42:39 (audience laughs)
42:41 If you've studied biochemistry,
42:43 you will have an anaphylactic reaction.
42:45 (audience laughs)
42:46 If you haven't studied biochemistry,
42:48 you will fall asleep.
42:50 So, what I'm gonna suggest that you all do
42:53 is just let me do my thing, to show you that,
42:55 at least it works, and just count the arrows.
42:59 Okay?
42:59 You can do that, right?
43:00 Can you count the arrows, it's not like counting sheep.
43:03 Okay, you can count the arrows, and just stick with me.
43:05 Just let me do my thing,
43:07 and let me show you why fructose is not glucose.
43:11 'Cause what the liver does to fructose
43:12 is really unique, and you've gotta
43:14 understand it to understand everything I've just told you.
43:18 So, number one, fructose is seven times
43:21 more likely than glucose to do that browning reaction.
43:24 The advanced glycation end-products.
43:26 The thing that happens on your grill, 43:28 happens in your arteries for the same reason.
43:30 You can actually see the color too,
43:32 the color change too.
43:33 Fructose does not suppress the hunger hormone.
43:35 There's a hormone that comes form your stomach
43:37 called ghrelin you've heard about, already.
43:40 So, if you preload a kid with a can of soda,
43:45 and then you let him loose at the fast food restaurant,
43:47 do they eat more, or do they eat less?
43:51 They eat more.
43:52 They just took on 150 calories, yet they eat more.
43:56 Reason?
43:57 'Cause fructose doesn't suppress
43:58 the hunger hormone ghrelin, so they eat more.
44:03 Acute fructose ingestion does not stimulate insulin,
44:06 because there's no receptor for fructose,
44:09 no transport for fructose on the beta cell
44:12 that makes insulin, so the insulin doesn't go up.
44:14 Well, if the insulin doesn't go up,
44:15 then leptin doesn't go up, and if leptin
44:17 doesn't go up, you're brain doesn't
44:18 see that you ate something.
44:20 Therefor, you eat more.
44:23 And finally, I'm gonna show you
44:24 liver hepatic fructose metabolism
44:26 is completely different between
44:28 fructose and glucose, completely different.
44:32 And I'm going to show you, before the evening is out,
44:35 that chronic fructose exposure alone,
44:38 nothing else, causes this thing
44:40 we call the metabolic syndrome.
44:41 Everybody knows what the metabolic syndrome is?
44:44 So, this is the conglomerate
44:46 of the following different phenomena,
44:49 obesity, Type 2 diabetes, lipid problems,
44:54 hypertension, and cardiovascular disease.
44:57 Those all cluster together, called metabolic syndrome.
45:02 I'm gonna show you how fructose does every one of those.
45:06 I wanna show you the difference between
45:07 glucose and fructose in a way that
45:10 will be glaringly apparent.
45:12 So, let's consume 120 calories in glucose.
45:17 Two slices of white bread.
45:19 What happens to that 120 calories?
45:22 You eat the 120 calories, 96 or 80%
45:26 of the total will be used by all the organs in the body.
45:30 80% off the table.
45:32 Why?
45:33 Because every cell in the body can use glucose.
45:37 Every bacteria can use glucose,
45:38 every living thing on the face of the earth
45:41 can use glucose, because glucose is the energy of life.
45:45 That's what we were supposed to eat.
45:48 24 of those calories, or 20% will hit the liver.
45:52 So let's watch what happens to those 24 calories.
45:55 Here they go.
45:56 So, the glucose comes in through this transporter
45:58 called Glut2, out here, the glucose
46:00 is gonna stimulate the pancreas to make insulin,
46:02 the insulin's gonna bind to it's receptor,
46:04 and it's gonna take this substrate over here
46:07 called IRS-1, insulin receptor substrate 1.
46:10 That's not important right now, don't worry.
46:11 And it's gonna tyrosine phosphorylate it.
46:14 And it's going to be tyrosine IRS-1,
46:16 which is now active, that's active.
46:18 And it's gonna stimulate the second
46:19 messenger here called AKT.
46:21 Now what AKT does is, it stimulates this guy down here.
46:24 SRABP1, sterol receptor binding protein number 1.
46:29 Don't worry about it.
46:30 But this is the thing that, ultimately,
46:31 gets fat mechanics going.
46:34 So, you 'll see in a minute.
46:36 So, one of the things that SRABP1 does,
46:38 is it activates this enzyme here called glucokinase,
46:40 which takes glucose to glucose 6 phosphate.
46:43 Now, glucose 6-phosphate can't get out of the liver.
46:46 The only way to get glucose 6-phosphate
46:47 out of the liver is with hormones.
46:49 Glucagon or epinephrine, that's the way it can get it out.
46:52 So now, the glucose is fixed in the cell,
46:54 but it's only 24 calories worth,
46:55 so it's not a big bolus of it.
46:59 Now, the glucose 6-phosphate
47:01 almost all of it, is gonna end up
47:02 going over here to something called glycagen.
47:05 Now, glycagen is the storage form of glucose in the liver.
47:10 Because glycagen's easy to fish the glucose out
47:12 with glucagon and epinephrine.
47:14 So, my question to you, and granted,
47:16 this is a physiology question,
47:18 is how much glycogen can your liver store
47:20 before it gets sick?
47:24 The answer's any amount.
47:26 It's unlimited.
47:28 We have carb loaders who run marathons, right?
47:33 Does it hurt them at all?
47:35 We have kids with a disease where they can't
47:37 get the glucose out of the glycagen,
47:39 called glycagen storage disease type 1A,
47:41 or von Gierke disease.
47:43 They got livers down to their knees their so big.
47:45 They're hypoglycemic like all get out 47:47 'cause they can't lift the glucose out of their liver.
47:49 But, they don't go into liver failure.
47:52 Because glycagen is a non-toxic storage
47:55 form of glucose in the liver.
47:57 So, the whole goal of glucose
47:59 is to replete your glycagen.
48:01 So, this is good, this is not bad, this is good.
48:04 Now, a little of that glucose is gonna fall down here,
48:08 it's gonna get metabolized down
48:09 to this stuff here, called pyruvate.
48:11 And the pyruvate is gonna
48:12 enter your mitochondria, over here.
48:14 Remember, your mitochondria are
48:15 the parts of your cell that actually burn the energy.
48:18 They're your little factories.
48:19 They make the stuff that lets you live.
48:23 Called ATP, ATP, adenosine triphosphate,
48:25 that's the energy of life, right there.
48:27 So, the pyruvate comes in, gets converted
48:29 to something called acetyl-CoA,
48:31 gets metabolized by this thing called
48:33 the Krebs cycle, TCA cycle, and you throw off
48:35 ATP and carbon dioxide which you breath off.
48:37 So far, so good?
48:39 Have I snowed anybody yet?
48:41 You're with me?
48:43 I snowed one guy back there.
48:44 (audience laughs)
48:45 I'm doin' my best, I swear to God,
48:46 I'm doing my best.
48:47 Anyway, so this stuff over here,
48:48 this acetyl-CoA, gets burned off in the TCA cycle.
48:53 Maybe you won't burn all of it off,
48:55 and so, some of it may exit as citrate.
48:58 And the citrate then leaves the mitochondria
49:00 through a process known as the citrate shuttle.
49:02 And then that citrate can then be broken down
49:05 by these three enzymes, which are all
49:06 subservient into this SRABP1.
49:09 This is ATP citrate lyase acetyl-CoA
49:11 carboxylase fatty acid synthase.
49:13 They're not important.
49:14 The only thing to know is these three
49:15 enzymes together turn sugar into fat.
49:19 This is called denovo, meaning new,
49:22 lipogenesis, fat making.
49:25 This is denovo lipogenesis.
49:27 So you take the citrate which came form the glucose,
49:30 and you end up with something called acetyl-CoA,
49:32 which then gets packaged with this protein here,
49:34 and you end up with something called VLDL,
49:38 very low density lipoprotein.
49:41 Now, anybody heard of that before?
49:44 Is it good or bad?
49:46 It's bad, that's bad.
49:48 VLDL is bad because that's one of
49:50 the things that causes heart disease.
49:52 It's also a substrate for obesity.
49:54 So, you don't wanna make much of this.
49:58 But the point is, you started with 24 calories,
50:01 maybe a half a calorie will end up as VLDL.
50:05 So, that little Japanese guy with the little hat,
50:08 you know, working out in the field,
50:09 eating rice for the next 90 years,
50:12 can he die of a heart attack at age 90?
50:15 Sure.
50:16 But that's not so bad.
50:18 If you make it to 90, you're doing alright.
50:20 Because that VLDL coming from glucose.
50:23 Glucose made a little bitty VLDL.
50:26 And that serves as a substrate for adipose deposition
50:29 into your fat cell, here triglyceride.
50:31 In addition, because of the insulin
50:33 went up in response to the glucose,
50:34 your brain sees that signal.
50:38 And it knows that that is supposed
50:39 to shut off further eating.
50:43 In other words, hey, I'm busy metabolizing my breakfast.
50:47 I don't need lunch.
50:50 And so, you have a nice negative feedback loop
50:53 between glucose consumption, the liver,
50:55 the pancreas, and the brain, to keep you
50:57 in normal negative, yin yang energy balance.
51:02 This is good, this is not dangerous.
51:05 This is what's supposed to happen.
51:07 So now, let's talk about a different carbohydrate.
51:11 Let's talk about my favorite carbohydrate, maybe yours too.
51:16 (crowd murmuring) 51:18Ethanol.
51:19Ethanol is a carbohydrate, isn't it?
51:21Here's the structure, carbon hydrogen oxygen,
51:24it' a carbohydrate.
51:26But, we all know that ethanol is a toxin, right?
51:29A poison, right.
51:31You can wrap your Lamborghini around a tree,
51:34or you can fry your liver, your choice.
51:37Depends on how much you drink and how often.
51:40Right? Okay.
51:42So, we know that ethanol is not good for you,
51:45except, of course, a little bit is good for you.
51:48So, we can talk about that too, later, if you want.
51:50But, let's talk about how it's bad for you.
51:53So, here's acute ethanol exposure.
51:57CNS depression, vasodilatation, hypothermia,
51:59tachycardia, myocardial depression,
52:01pupillary responses, respiratory depression,
52:03diuresis, hypoglycemia, loss of fine motor control,
52:06you all went to college.
52:08(audience laughs)
52:10Here's fructose, nothing.
52:13It doesn't do any of those.
52:13Because the brain doesn't metabolize fructose.
52:17Alcohol gets metabolized in the brain,
52:19to cause all of those things, but fructose doesn't.
52:22So, fructose is not an acute toxin, ethanol is.
52:26We control ethanol, don't we?
52:29We have something called
52:30the Bureau of Alcohol Tobacco and Firearms.
52:33We have all sorts of things, we tax ethanol.
52:35We do all sorts of things to limit consumption of ethanol.
52:39The Nordic countries, all the liquor stores are state run
52:43in attempt to try to set the price of ethanol high enough
52:47so as to discourage consumption for public health reasons.
52:51We have 1500 years of alcohol control policy in this world
52:55to draw on, in terms of how to limit consumption.
53:00Got it?
53:01Because ethanol is a toxin, and we know it.
53:05So, let's consume 120 calories in ethanol.
53:10Shot of Makers Mark.
53:13Anybody taste it?
53:14Yeah, good, okay.
53:15So, 24 calories right off the top.
53:19The stomach and the intestine have something
53:21called the first pass effect, so 10% off the top,
53:24and kidney, muscle, brain will consume the other 10%.
53:28So there goes 20% or 24 calories right off the top.
53:3196 calories of the 120 are gonna hit the liver.
53:35Now, how many was it for glucose?
53:37It was 24.
53:39So, four times the substrate is gonna hit the liver,
53:43and there's the rub.
53:44This is a volume issue.
53:46We're gonna show you how.
53:48So, the ethanol comes in, passive diffusion,
53:51there's not receptor for it, not transporter.
53:54First thing that happens is ethanol
53:55gets converted to this guy, over here, called acetaldehyde.
54:00Anybody know anything about aldehydes?
54:02Like formaldehyde? Right?
54:05Are aldehydes good for you or bad for you?
54:07They're bad, right?
54:09'Cause what do they do?
54:11They can cause cancer, they cross link
54:13proteins is what they do.
54:14So, if you cross link enough proteins in your liver,
54:17what do you think happens to it?
54:19You get something called...
54:21Cirrhosis, right exactly.
54:23So this guy, over here, is bad.
54:25And it generates something called reactive oxygen species.
54:28Reactive oxygen species damage proteins in the liver.
54:32And the more alcohol you drink,
54:33the more of this stuff you get.
54:36So far, so good?
54:37So, this is one of the reasons why alcohol's bad.
54:40Now the acetaldehyde will come down here
54:42to something called acetate.
54:44The acetate will enter the mitochondria,
54:46just like the pyruvate did before.
54:48Will get converted to acetyl-CoA
54:49and participate in the TCA cycle,
54:50just like before, to generate energy.
54:54So that alcoholics don't die form lack of energy,
54:58they got energy, it's everything else they don't have.
55:00They're gonna have a whole lot of citrate.
55:03Because they have 96 calories that
55:06have to get metabolized.
55:07How many calories made it to the mitochondria with glucose?
55:13About half, right?
55:15Because most of it went to glycogen.
55:17So, we've got a big citrate, so it's in big font
55:20to show you that we're talking about big citrate now.
55:23And so, the big citrate is gonna get metabolized
55:25all the way to VLDL by the CRABP1.
55:28And so you're gonna get a lot of the LDL.
55:29And this is the dyslipodemia of alcoholism, right here.
55:34Everybody see that?
55:35So, the liver's gonna try to export
55:37this VLDL out so that it doesn't get sick,
55:40because when fat builds up in the liver,
55:42that's not good for it.
55:45Some of it's gonna exit as free fatty acids,
55:47and those free fatty acids, will take up residence
55:49in the muscle, and you get something
55:50called muscle insulin resistance.
55:52So insulin resistance, that's a bad thing.
55:54That makes your muscles and your liver now work so well.
55:58And can cause all sorts of other problems like diabetes.
56:01Some of the acetyl-CoA won't even make it out,
56:03and will precipitate as a lipid droplet,
56:05so there's your alcoholic steatohepatitis.
56:11This acetyl-CoA, and this ethanol,
56:13and these reactive oxygen species
56:14can start this enzyme activated.
56:18It's called c-jun n-terminal kinase 1,
56:21or JNK1, and it really is JNK1
56:23because it is the bridge between
56:26metabolism and inflammation.
56:28So, when you generate JNK1, you do bad things to your liver,
56:32which I will show you when we talk about fructose.
56:35So let's talk about fructose.
56:37Fructose is sweet, we like it a lot.
56:39We like it in everything, we like it in our bread,
56:41we like it in our pretzels, we like it everywhere we look.
56:45So, let's consume 120 calories in sucrose.
56:50A glass of orange juice.
56:52Everybody got it?
56:53So, two slices of white bread, a shot of makers mark,
56:56a glass of orange juice, all the same 120 calories.
57:01But, three different substrates.
57:05Let's see what happens to the fructose.
57:07So, number one, the glucose, remember,
57:10'cause sucrose is half glucose half fructose,
57:12so 60 of the calories of the 120 are glucose.
57:1612 are gonna make it into the liver,
57:1848 out here for the rest of the body.
57:20The same 20/80 split we had before with glucose.
57:24So far, so good.
57:25But all 60 calories of fructose are
57:27gonna be metabolized by the liver.
57:29Because only the liver can metabolize fructose.
57:33So, what do we call it, where when you
57:35take in a compound that's foreign to your body,
57:38and only the liver can metabolize it,
57:40and in the process, generates various problems?
57:45What do we call that?
57:46We call that a...
57:49Poison. 57:50So, let me show you how it's a poison. 57:53So, let's watch the fructose. 57:55So, the fructose comes in through this transporter, now. 57:57Before it was Glut2, now it's Glut5 58:00No insulin, remember, 'cause fructose 58:02does not stimulate insulin. 58:04Fructose, then, gets metabolized by this guy, over here, 58:07called fructokinase, to form something
58:09called fructose 1-phosphate. 58:11In the process, ATP has to give up 58:14one phosphate to ADP 'cause the phosphate
58:16had to come from somewhere, so it comes from here.
58:18Now, before we had 24 calories 58:21that had to be phosphorylated. 58:23Now we have 72 calories that have to be phosphorylated. 58:27So, we have three times the substrate, 58:29and there's the rub.
58:31It's a volume issue, for right now. 58:33So, we're gonna lose a lot of phosphate, aren't we?
58:35So there's a scavenger enzyme in your liver 58:37called AMP deaminase 1 to rescue 58:40the phosphates off the rest of the ATP molecule, 58:44and it takes ADP down to AMP, adenosine monophosphate, 58:47down to IMP, Inositol monophosphatase, 58:50and finally, to the waste product uric acid. 58:53Anybody every heard of uric acid? 58:56What is it?
58:59It's a waste product. 59:00Goes out in your urine.
59:01'Causes what disease?
59:03Gout, right. 59:06Also causes another disease called hypertension. 59:11Let me show you how. 59:13Because uric acid, turns out, blocks 59:15the enzyme in your blood vessels
59:17called endothelial nitric oxide synthase.
59:20And that's the enzyme that makes 59:21the stuff called nitric oxide, NO.
59:23And that is your endogenous blood pressure lowerer.
59:27That keeps your blood pressure low.
59:31So, when you can't make it, your blood pressure goes up.
59:35So, this just shows that fructose consumption 59:37increases gout in adults.
59:39So, this is a study that came out last year 59:41showing that fructose consumption
59:43increases the risk for gout, 59:46showing that uric acid's going up. 59:48And this is a study done by pediatric renal fellow, 59:50Stephanie Winn, just published in
59:52Journal of Pediatrics,
59:53it's not submitted any more, it's long in press, 59:56showing that this is in the NHANES database
59:59in the adolescents, showing that sugar sweetened beverages, 60:02as it goes up, your uric acid goes up.
60:06And, not only does your uric acid go up, 60:09but here's your sugar sweetened beverages,
60:10and here's your systolic blood pressure going up.

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