Episode 161: Dr. Naim Akhtar Khan

Dr. Naim Khan is a Professor of Physiology (Exceptional Class) at Burgundy University, Dijon (France). He is the Head of a Nutritional Physiology & Toxicology research team affiliated with the Inserm Research Center (UMR1231). He is the principal (co) author of more than 250 research peer-reviewed articles. He is the Editor of Nutrients, PlosOne, and J Clin Med. He has been a visiting professor at U Chiba, Japan, and U Cagliari, Italy. He is a Fellow of the Royal Society of Biology, UK. He has been Innolec laureate at Masaryk University, Czech Republic; awarded the Robert Naqué Prize by the Société de Physiologie (France); Nutrition & Food Excellence Prize by the National Academy of Medicine (France) and nominated as Ambassador for Research by the Burgundy State (France). He founded a start-up, “Ektah,” that obtained the iLab Prize (France).

Dr Khan has been Secretary General and is acting as Secretary for International Affairs at the Société de Physiologie (France). He is a founding member of the African Society of Physiology and Physiopathology, Senegal. He is an expert member in commissions like ATRBSA Algeria, National ANR France, InnovIris Belgium, and National Agency for Food Security (Anses) France. He has collaborated on obesity physiology with India, Morocco, Tunisia, Benin, Senegal, and Ivory Coast. We at Food Junkies are especially interested in his review of the literature on fat addiction.

The content of our show is educational only. It does not supplement or supersede your healthcare provider's professional relationship and direction. Always seek the advice of your physician or other qualified mental health providers with any questions you may have regarding a medical condition, substance use disorder, or mental health concern.

TRANSCRIPTION

My name is Dr. Vera Tarman and I am your host today speaking with Dr. Naeem Akhtar Khan, a researcher who claims that fat alone can be addictive even when not in connection with sugar. Dr. Naeem Khan is Professor of Physiology at Burgundy University, Dijon, France. He is head of a research team in nutritional physiology and toxicology and is principal co-author of more than 250 research peer-reviewed articles and a number of scientific books, many focusing on diet-induced obesity factors. He is editor of Nutrients, Paws 1, and Journal of Clinical Medicine. He is a fellow of the Royal Society of Biologists. So we at Food Junkies are especially interested in his review of the literature on fat and fatty food addiction. Yes, we know about sugar, but what about fat? So, welcome Dr. Naeem Khan.

2
0:01:44
Can you start by just telling us a little bit of the personal story? What got you interested in the whole idea about researching fatty food addiction?

1
0:01:53
First, I would like to express my thanks to you for giving this possibility to talk about our research work and research interests. I was interested in obesity as there are many people who are obese in my family. My mother was obese. She always used to say that she did not eat well, still she was obese. This point hit to my mind when I was a child, how a person who did not eat a lot could be obese. And this is how my journey started from obesity to fat addiction and research.

2
0:02:26
Thank you. Can you give us an idea of what kind of research are you doing or have you done?

1
0:02:30
Yeah, at the moment we are working on anti-obesity strategies. We are advocating that there might be a sixth sense of taste, the taste for fat. We have identified in the TENC-PAPILY the fat taste receptors like CD36 and GPR120 whose expression is downregulated in most of the obese and therefore there is less or a sensory detection of dietary fat.

2
0:02:54
So you're claiming that there are six taste receptors in the tongue. So there's salty, there's umami, there's sugar, sour and fat.

8
0:03:04
And acid.

2
0:03:05
And fat as well.

1
0:03:07
Yeah, fat is a sixth one.

2
0:03:08
Yes. Interesting. You'll tell us more about that. Before we get into it, just as a curiosity, where are you getting the research funding for this? Because the concept that there's a sick ingredient that might be making foods addictive, surely the food industry is not funding this. So who would fund something like this?

1
0:03:24
Yeah, you're right. Certainly food industries, they are not very close friends to us in this context. But our research is funded by regional, central government, and EU grants obtained through CAR proposals. We also collaborate for clinical work with different African teams through bilateral

2
0:03:45
grants. Thank you. So let's delve into this whole area of fat addiction and the physiological and the psychological aspects of that because we've been talking about sugar addiction in our food addiction world endlessly and a lot of people will say fat not addictive. My first question to you, are you looking at studies specifically looking at fat and are you looking at foods that are without sugar so that there's no confounding variable of the sugar?

1
0:04:13
Yeah, the first thing is that fatty food addiction can be identified on the basis of distinct features of salience and inability to control the intake of specific types of food. That's very similar to the addiction to psychoactive substances. In fact, fat binge eating is very similar to sweet binge eating, as both are associated with dopamine signaling within the mesolambic reward circuit. However, there is a co-founding factor that high fat eating may lead to increased weight gain and adiposity. And this is not true for sugar addiction. So there are differences, but there are some common features too.

2
0:04:52
I just want to clarify for our listeners, when you're looking at foods that are high in fat, there's no carbohydrates or sugar that could be confounding the question.

1
0:05:01
Yeah, we have conducted studies in animals but in human beings it's very difficult to attribute that it is only due to the presence of fat. But we did questionnaire and we asked the obese subjects and we deduced that they were indeed talking about fat and fat-derived substances.

2
0:05:23
Can you give an example of what kinds of fatty foods could be addictive that don't have sugar, like fatty meats for example?

1
0:05:30
Some foods with no carbohydrates, like steak and bacon, have a lower addictive potential or neural reward activation as compared to addictive drugs. Take an example, the products like tobacco are also in the same category. Low reward products trigger addiction in the long run. There is clear evidence that dietary fatty acids do activate the reward system through otosensory and gut-to-brain pathways. The loss of control over consumption is a feature of addictive eating, the bacon, cheese, nuts and steak are naturally high in fat. The loss of control ratings for them was lesser than processed food, but higher than chicken breast and vegetables.

2
0:06:14
Okay, alright. So on a continuum, processed foods would be the highest, but bacon and steak and cheese would still have some addictive potential more than regular foods like vegetables.

1
0:06:27
Highly processed foods like pizza, ice cream, white bread, cookies, chips are very addictive as they contain refined carbohydrates and fat. These foods are highly reinforcing and some individuals consume them compulsively.

2
0:06:41
Yes, but could you compulsively eat too much bacon and steak and cheese?

1
0:06:46
Not so much, but in the long run, of course for example as I try to compare tobacco and cocaine or morphine yes both of the categories trigger addiction but in a different way for example drug is very active to trigger reward circuit but tobacco nothing when we start smoking when somebody offers a cigarette and you don't start smoking immediately by and by you smoke you become addicted. Smoking or tobacco has a lower addictive potential. The same thing is for nuts and bacon and meat. There's a lesser addictive potential, but in the long run, they will also trigger addictive eating behavior.

2
0:07:30
That's interesting news for our keto community, where sometimes that's all they're eating is that kind of fatty foods. In fact, they often encourage fatty foods because they want the fat to replace the sugar for satiation. But you're saying that if a person is predisposed to addiction, they could be in trouble with those foods.

1
0:07:49
Yeah, this is very interesting because people say we should take a food without sugar and all the day they try to avoid sugar. But sugar is very important for the body. For example, I'm talking to you. My brain will use 5 grams of sugar per hour. In one hour of an interview, my brain, only the brain, will require 5 grams. I'm not talking about the whole body. That's the reason we should take sugar, but in a controlled way.

2
0:08:18
If I can challenge you, the keto people will say, after a certain point, we don't need any sugar because we can rely on our ketones for our brain energy source.

1
0:08:27
Yeah, the problem is here. Yes, I agree with you. But if you take less carbohydrates, less sugar, and more meat, or meat-derived substances, the higher the intake of meat, the higher is the intake of amino acids. It means you will produce more and more urea and ammonia. So there will be a high renal load. So why are you increasing the renal load? So while you are increasing your renal load, it may trigger some diseases like gout disease or other diseases because the concentrations of urea and ammonia in the body, the higher the function of the liver to remove and to transform it into glutamic acid and glutamine. This overload is not good for our bodies.

1
0:09:09
Physiologically, and I'm a physiologist, it's not good.

2
0:09:12
Rather, we should have a balanced diet. You would not be an advocate of the keto diet then, one where the carbohydrates are under 20 grams of carbohydrates for example?

1
0:09:19
Yeah, I will not advocate it. Okay. Another point is this, the person who will be on keto diets or carnivore diets, they will have less vitamins. And vitamins are important for our growth, for maintenance of our body. And this, how can we take it? We ignore completely this point.

2
0:09:38
Related to that, one of the things that people talk about in the keto community is something called fat intolerance. Do you know anything about that phenomena where people eat a lot of saturated fat? Some people have a problem with excess saturated fat. It makes them nauseous, it makes them tired, it makes them fatigued, headache. Do you know what that's about?

1
0:09:57
Yeah, saturated fat is not good in the excess quantity, of course. Yeah, we know that. Palmitic acid for example, it induces insulin resistance in a number of models and trans fatty acids also contribute to deterioration of insulin sensitivity and we know that prolonged intake of acid or palmitic acid rich diets reduces mesolimbic dopamine energy signaling and sensitivity to the rewarding effect of amphetamines. So saturated fatty acids also favor insulin resistance and that's not good for health.

2
0:10:31
I'd like to ask about that. My understanding is that excess sugar, I'm talking like added sugar, far more than the pancreas and the liver can manage will cause insulin resistance. But you're saying that fat itself can also cause insulin resistance. Can you explain that?

1
0:10:46
Yeah, particularly saturated fatty acids. We're talking about monounsaturated fatty acids like palm oil. That's good quantity because we should have a balanced monounsaturated, polyunsaturated and saturated fat. But if we have excess of saturated fatty acids they will trigger the activation of IKKB and TORS signaling in hepatocytes, macrophages and protocytes and will trigger insulin resistance in these models and that's bad for health. It's not because there's too much sugar that's demanding more insulin. Yeah it's nothing to do with that. We are talking about saturated fatty acids not about sugar because sugar of course in excess triggers insulin resistance we know that but fatty acids they are ingested incorporated in the plasma membrane and particularly in the phospholipids and therefore will interfere with insulin signaling the receptor to insulin and this interaction with signaling cascade of insulin will render

1
0:11:52
insulin receptors inactive. Okay. So this is how we can say insulin resistance means the receptor functioning of insulin is not working well. This can be done by saturated fat.

2
0:12:06
That's interesting. That's an extra piece of information about what can contribute to insulin resistance. It's very interesting because we've been focusing on how insulin resistance is created by excess sugar but you're saying saturated fat, not all fats, but excess saturated fat can also

1
0:12:22
affect the insulin receptors and therefore create insulin resistance. One should be careful about fat, whether it's saturated or unsaturated in terms of calories. Fat is fat. One should be careful about fat. Ultimately, all kinds of fat in excess are bad for health. One of the

2
0:12:41
reasons that people talk about eating fat instead of sugar is that it satiates. If you're not eating sugar, then you're going to be hungry because complex carbohydrates may not be filling. Some people make the argument that carbohydrates just make you more hungry but it's fat that is satiating partly because of how it affects the hormones. Can you comment on what the role of fat is in leptin and ghrelin?

1
0:13:03
Now chronic high-fat diet give to animals a persistent inhibitory effect on plasma ghrelin levels. It exerts an inhibitory effect on ghrelin concentrations. Another point is that ghrelin is not only released from stomach epithelium, but also taste buds. And we know that taste buds not only synthesize ghrelin, but also express ghrelin receptors. So ghrelin in the buccal cavity is modulating fat taste perception, transmitting the information on fat arrival in the mouth to the brain and in the brain to the reward system.

2
0:13:42
So you're saying that the moment you put a bit of fat in your mouth you're already starting to get hungry and desire more fat.

1
0:13:49
Exactly. Fat taste receptors in the mouth, I mean in taste buds cells, are playing a role, I should say, before the brain is very important to activate brain-gut axis and ghrelin is playing a role at first hand in the mouth at the papillae level

2
0:14:12
and ghrelin tells you that you're hungry even just by virtue of putting the food into your mouth

1
0:14:17
I would like to say the ghrelin is amplifying fat signal and the brain says hey fat is coming let's prepare

2
0:14:25
yes okay I guess it's the concept of the appetizer you put an appetizer in your mouth and now you want more but you're going to want more fat I guess. What about leptin how does that affect leptin? Leptin being our satiety hormone the hormone that makes us feel full at the end of a meal. Leptin and

1
0:14:41
leptin resistance are playing important roles in fat addition. At first hand as I As I said, the ghrelin is secreted by TACE-BAR cells. The same thing is the leptin. We have demonstrated that the cells that express FET-Tase receptors do express leptin receptors. The leptin is somehow playing an autokinetic role in the regulation of FET-Tase perception in the mouth. And the decreased leptin amount, some sort of leptin resistance in the mouth, will further influence food intake, particularly fatty food intake. But how does the leptin resistance occur?

1
0:15:17
Leptin resistance is action at different levels. Leptin receptors are expressed by lateral hypothalamus and also in ventral trigeminal area. Leptin administration suppresses feeding by acting on GABA neurons. Secondly, leptin administration reduces feeding and dopamine release within nucleus and chamas, thus exerting a suppression action against food-induced reward. Tinnitus is associated with high cannabinoid levels and high orexin in the neurons. And we know that cannabinoids and orexins trigger food intake. And it has been shown that administration of orexins

1
0:15:57
into ventral pigmental area increases dopamine release.

2
0:16:02
So that's leptin resistance. So is there a sweet spot as it were with eating fat where it is satiating but then it becomes non-satiating, it becomes addictive? Is this a case for moderation where you can eat so much so that the leptin kicks in and makes you feel that's its job? But then if you eat too much you can become resistant.

1
0:16:21
Yes, but in this case if we are in leptin resistance there is a direct activation of the reward system because leptin resistance is leading to high cannabinoid levels.

2
0:16:34
But how do you get to leptin resistance?

1
0:16:36
Not much is known. The scientists directly administer leptin into the brain and then they measure dopamine release and they identify neurons expressing the receptors for leptin in the rat model.

2
0:16:49
Is there implication that eating too much fat can lead to

1
0:16:52
leptin resistance? Yeah, because we know that in some cases leptin receptors are downregulated in our plate nucleus and nucleus and compounds. Getting back to

2
0:17:04
the addictive nature of fats, I read that the saturated fats are more addictive

1
0:17:09
than the poly and the monosaturated fats. Can you speak to that? Yeah, as I said that saturated fatty acids, they are more addictive because they exert their action at different levels. They trigger the activation of the dopaminergic system and they also bring more calories and they trigger hyperinsulinemia. This is how they trigger insulin resistance

2
0:17:35
and that will lead to addictive nature. Now let's get back to your discovery about the taste receptors genetics may predispose a person to fat addiction at

1
0:17:45
this level is that true? Yeah we conducted a number of clinical studies in obese and non obese children, adolescents and adults in different countries like Algeria, Morocco, France, Czech Republic and Senegal and Tunisia and in France. You know why? Because obesity is different in different countries because what we eat in Algeria and Tunisia we don't eat in France, in Czech Republic. So a Czech obese will be different from Arabic obese. Oh really? Can you explain that more? That's very interesting. Phenotypically they are the same by apparent look, but the factor that are inducing obesity in Arabic it's more sugar and more fat but in a Czech person he is not eating more fat but larder is a lifestyle he has different one so we tried to compare now we are working with Indian population vegetarian population and in the other 600 people that do not eat meat they rather feed only vegetables still some of them are obese and it's increasing. So how come a vegetarian is

1
0:18:52
becoming obese? It's the same but some difference will be in the mechanisms. And what about a fat taste? And we observe that in these countries that I have cited that obesity is associated with a less or a sensory perception of fat in the obese. Some of them have genetic predisposition, there's an association of fatty acid taste receptor, high fat intake, and obesity.

2
0:19:19
So, the vegetarian in India has a genetic predisposition to eating more fatty foods in the vegetarian foods? Why is it that in Arab...

7
0:19:28
I agree with you.

1
0:19:29
There are two aspects. One is genetic aspect. Some of them have genetic predisposition of CD36 gene polymorphism. One of my students from a lab trained in France went back to India

2
0:19:41
published a paper on this subject. If they have that genetic predisposition, what are they eating that's different than somebody else? Yeah. What's happening to their body that's different? Yeah,

1
0:19:51
that's different because polymorphism is not only involved in taste perception but also in beta oxidation in the body and also in the burning of fat in the liver and the soakage of fat in the adipose tissue. And these subjects, they had different diet patterns because dietary habits are also important. Being vegetarian, they eat a lot of fat derived from milk. Other, we call butter or clear butter. That's very obesogenic. And in India, according to culture or lifestyle, people love to eat butter or clear butter. So what you're saying then

2
0:20:29
is that the person's genetic predisposition not only may make them more vulnerable to fat addiction but also how the fat is being metabolized it might make them more likely to become obese than another similar person that is eating the same foods who may not become obese. Yes and this was our idea

1
0:20:47
we are working on and parallel we are trying to develop a kind of kit to detect the genetic polymorphism in the newborn babies. The idea is if we could make this kit and we go to the gynecology department where the children are born, they are diagnosed for some diseases. Anyhow, we can tell them whether the baby is suffering from genetic polymorphism for CD36. And we can ask the parents to take care about their dietary habits, about lifestyle of their children. They are prone to develop obesity.

2
0:21:30
Would you be able to say to them, because they're prone to develop obesity, avoid dairy fats, for example, or avoid saturated fats. But somebody else might not have to worry as much.

1
0:21:42
Yes, you're right. But one point is also here and I would like to make it clear that one subject who has no genetic polymorphism of serotherastics, he becomes obese for overeating or because of social, economic circumstances. That's not associated with a down regulation of fatty receptor in the tank. In Australia, it has shown that when obese women go for dieting for eight weeks, the receptor that's down regulated comes up. That is the reason when we do some dieting, we lose weight and then in the beginning we don't like eating fat. It's not we don't like eating fat. No, it's because the receptor which is down regulated during obesity is upregulated after a dieting.

2
0:22:36
And so then you don't need as much fat to taste the fat.

6
0:22:40
Exactly.

2
0:22:41
You're more sensitive to the taste.

1
0:22:43
Exactly.

2
0:22:44
Presumably if you're eating a lot of fat you down regulate and you lose the sensitivity and want more to gain that back. Exactly you're right. That's part of the concept of the addictive pathway of fat itself. So there's this the taste in the tongue but there's the vagal intestinal fat sensing. Can you

1
0:23:02
talk to that? Yeah. Intestinal vagal input plays an important role in sensing of dietary. The gut lipid sensing communicates to striatum. Indeed Indeed, surgical resection of vagus nerve prevents stimulation of dopamine release. Vagal neurons respond to intestine delivery of fat, particularly small intestine, jejunum. The upper part, close to the duodenum, is involved in lipid sensing and suppresses protein take through the release of anorectic peptides like CCK and GFP1.

2
0:23:34
Anorectic, meaning you're not hungry anymore.

1
0:23:37
Yes. But in the obese, we have observed that the less lipid sensing, the message on lipid detection in the intestine is downregulated.

2
0:23:47
Right, so they don't become satiated as quickly.

1
0:23:50
Exactly. And it goes to the brain. So less secretion of anodic peptide means less satiation, means again the whole system in a very organized way. Tongue, brain, gut, which is down regulated during excessive fat eating behavior.

2
0:24:07
But it sounds like again that a certain amount of fat is helpful but then you can cross the line and then it works against you. Yes. Because of the resistance factor.

1
0:24:17
And we have observed when we have intestinal cell lines in the laboratory and taste buds cell lines from two origins with fat, the fat sensors go down. The higher we eat the fatty substances, the lower is the sensing and the eating behavior going up and up, it will lead to fat addiction. Yes, now you mentioned the endocannabinoids, they are fantastic molecules. Like we know, tetrahydrocannabinol at low doses induces hyperphagia.

2
0:24:58
Yes, makes you want to eat a lot, and go to the munchies.

1
0:25:01
Yes, and the endocannabinoid stimulates food intake, particularly intake of sugars and fat. Now, it is known that endocannabinoid seniline regulates synaptic plasticity both in hypothalamus which possesses hunger center and mesolimbic center thus affecting both the pummy function and interestingly there is a cross talk between leptin and ghrelin and the two cannabinoids are regulating food rewire process. The upregulating behavior and addictive behavior appears. Can you speak to the hyperpalatability about fat. Yeah, I'd like to say that fat confers textural and creaminess to food and makes it more palatable. So from the appearance and the tasting level, food becomes palatable and food is consumed across all ages from infancy to adulthood to elderly. Evolutionarily, this confers survival and benefit to human beings. However, a rich diet induces insulin secretion and we know that insulin infusion modulates palatability.

2
0:26:09
Now, how does fat create insulin production?

1
0:26:12
Yeah, because when you take excess of fat and you are taking less sugar and your body requires sugar, in this case, then some glycogen is converted into the glucose and fat which is stored into the form glycogen is giving to sugar. Fat is giving rise to insulin secretion indirectly.

2
0:26:33
Got it. By the glycogen.

1
0:26:35
Yes. Fat activates sympathetic nervous system. And insulin secretion via brain is called PVN, paraventricular nucleus, that is directly connected to pancreas. And fat stimulates this system and induces the release of insulin.

2
0:26:51
So if I can summarize this, sugar will directly affect insulin stimulation, but fat does it indirectly.

1
0:26:59
Yes.

2
0:27:00
Yes.

1
0:27:01
And we know that insulin induces palatability.

2
0:27:04
And fat storage.

6
0:27:05
Yes, of course.

2
0:27:06
Okay, let's talk about interventions now. You've discovered a fair amount about the taste receptors, the six taste receptors, the sixth place receptor and the intestinal fat sensing and also that there's a genetic predisposition. What are some interventions that you're

1
0:27:23
interested in that can help with the obesity crisis? Healthcare policies, for example in France, the ministry has launched a program by opening CSO, Centre Spécialisé de l'Obesité. Obese subjects are admitted there. They are offered psychological and psychiatric counseling, metabolic counseling, and even sports are offered.

2
0:27:43
Okay.

1
0:27:43
So we should take care of an obese in different point of view. I think one drug cannot help, like we are talking about GLP-1.

2
0:27:52
Yes, for example.

5
0:27:53
Yes, you're right.

1
0:27:54
GLP-1 agonists, receptor agonists, improve glycemic control, stimulate satiety, suppress appetite, and decrease body weight. And we know that they also decrease inflammation. But how they can decrease fat addictive behavior, it's too early to say.

2
0:28:11
Do they at all?

1
0:28:13
They talk about decreasing body weight. It's more commercial, but I'm afraid that GFP1 receptor agonist might have in the long run some adverse effects. For example, thyroid. C cells in the thyroid express high numbers of GLP-1 receptors. One should be very careful about the role of GLP-1 agonist.

2
0:28:32
Does it decrease the taste for fatty foods or the craving for fatty foods at least in the initial phase?

1
0:28:38
Yeah, we have not yet.

2
0:28:40
Okay, all right. So you're urging caution in the long term about these because we don't know where else the GLP-1's inhibition could be affecting our body.

1
0:28:50
What is also there that not every obese responds to GLP-1 agonists.

2
0:28:56
That's true.

1
0:28:57
There are responders and non-responders. A medical doctor is giving GLP-1 agonists and he says if the patient does not respond in a month still all obese are not sensitive to these agonists and we completely ignore this point because we are going more commercially and we are the victim of this kind of way that this is the magic or miraculous part against obesity and can be used to treat all

2
0:29:29
complications released with obesity. What about surgical options where they're removing or bypassing important parts of the bowel. Is there any impact there on?

1
0:29:41
Yeah, we know that the surgery-induced weight loss decreased food cravings in food addict subjects. We have conducted some experiments in mice, and we did vertical steel gastrectomy. And we observed that in these mice, there was increased otosensory detection of fat after weight loss. So what we can say, that decreased sensory part during obesity is reversed after bariatric surgery. That's a good point.

2
0:30:10
So you've had the experience, or at least with mice, that after surgery mice become less addicted to food. Exactly. But I've had the experience in clinical practice that a lot of people with post-periodic surgery become addicted, like first of all to alcohol and then to sugars, maybe not right away but after a year or two. So what's happening there then?

1
0:30:33
Our body in the obese situation is requiring some quantity of energies to maintain the body. Immediately we baptize a bariatric surgery. So the body which is habituated to have a number of calories for its maintenance is deprived of these calories. That is the reason that the person after bioreactive surgery is feeling very lethargic and sometimes some psychological problems and sometimes with sarcopenia. So we can say some nutrition-related problems arise that we ignore because what we know today and we try to emphasize to the general public, hey bioreactive surgery is giving less food intake, less food intake means less calories means body weight is lost that's fine. Are other associated complications in long run? I have seen some patients during last couple of 15 days I was in Algeria I met people which had bariatric surgery 10 years before. Yeah. Most of them become obese again because this is a if you let me explain, set point happens. During inflammation there is a neural

1
0:31:41
inflammation in the brain. So obesity and neural inflammation are associated together and during obesity neural inflammation makes some neural plastic connections which are neural and makes an energy set point very high. When you lose body weight because of dieting or bariatric surgery the brain says hey continue eating you have to come to this fat point. That is the reason there is a failure. And in the long run, you become again obese. Now, for example, you are taking three times in a day, then you take four times a day. Because the body is requiring calories.

2
0:32:14
Right, okay. So the final intervention, which would just be, what is the best diet that you would promote where you get the nurturing effect of fat, the satiety effect, but not the overabundance, which leads to obesity and fat addiction.

1
0:32:27
Yeah, I cannot recommend any diet but I can say personally a vegetarian diet that is balanced is good for health and one should be very careful about vegetarian. In Europe there is a tendency to go towards vegetarian lifestyle but people don't know what is a vegetarian lifestyle. We should when a vegetarian eats food in its food, there's yogurt, there's lentils, a source of iron, there is vegetable and bread and everything is controlled way. So if we have a balanced vegetarian diet, I think it will help us a lot. And where does the fat fit into that vegetarian diet? Yeah, fat is there, but in a small quantity because we take thrice a day milk or milk-dry products. What about olive oil, something like that yeah olive oil is is oil as I said and fat is fat yes okay calories now the better part of olive oil is that it is full of

1
0:33:23
monounsaturated fatty acids and these fatty acids enter competition in the hepatocytes I mean in the liver and in the enzymes that are involved in the synthesis of polyunsaturated fatty acids so monounsaturated fatty acids enter competition in the synthesis of polyacetate fatties in the liver and therefore decrease liver levels. That is a good part of olive oil.

2
0:33:46
Now, just in closing, what research are you doing now? What's your sort of latest interest?

1
0:33:52
Now, we have some fatty acid receptor agonists. And these agonists bring no calories, no toxic effects, they trigger early activation of fatty receptors just by local application in the mouth and the brain gets information, hey fatty food is coming and immediately there's high

2
0:34:13
secretion of anorexic peptides. Okay, you're fooling your brain that you're eating fat so

1
0:34:18
that you don't need to eat more. This is how we obtain early satiation. Wow. That means low low-fat food intake. Yeah, we are going towards the license. It will take time, not more than 2030. Wow. By now we have done a clinical study in Nantes, and that's very favorable. We'll start the phase one trial in obese in a different country. I cannot say now here if everything goes fine. We'll have another approach to decrease fat eating behavior and obesity rather than manipulating diets. Because when we eat some food today, we don't eat because we require calories. We eat for pleasure. We go to restaurants for the pleasure. And that is the reason obesity is going up and up arithmetically. Because we live only once. We want to enjoy life.

1
0:35:11
And when we even do dieting, we are tired of it. No, let's go out and have some good food. By our system, by our agonist, before going to a restaurant, just apply a spray in the mouth, especially receptors, appreciate your food. And you say, hey, this is a delicious food. But since you have early situation, you will less eat, means you will say, yeah, I'm satisfied.

2
0:35:34
Wow, so that one plate will be enough and then you're done.

1
0:35:38
Yeah.

2
0:35:39
That's a great idea. That's a great idea because you still enjoy your food. Unlike Ozempe, where a lot of people say they just don't enjoy their food at all. That's why they don't want to eat.

1
0:35:48
And psychologically, a human being doesn't want that his life should be controlled. He wants to master his life psychologically. So when I say eat what you want, go where you want, go on holidays on the beach eat whatever is there enjoy just give a fast information to the brain that fat is there.

2
0:36:07
Good, thank you. I have one more question and then we'll finish off but this is our signature question. If you could tell a younger version about yourself about fat or fat addiction what would it be?

1
0:36:18
I would like to say a very simple answer that's eat and enjoy. We live only once just take care of what you eat yourself and your beloved ones.

2
0:36:28
All right, thank you. Thank you so much Dr. Khan for your time and explaining what's quite a complicated system but you have convinced me that fat is a separate dynamic in the addiction profile and that we need to look at that. Thank you very much.

1
0:36:43
Thank you very much so as a few for having me invited here today. Thank you.

3
0:36:48
Thanks for joining us this week on Food Junkies, Recovery from Food Addiction. Make sure to join our Facebook group, Sugar-Free for Life Support Group, I'm Sweet Enough. You can subscribe to our show in iTunes or Stitchers, that way you'll never miss an episode. While you're at it, if you found value in this show, we'd appreciate a rating on iTunes. Or if you'd simply tell a friend about the show, that would help us out too. Don't forget to pick up your copy of Dr. Tarman's book Food Junkies, which is available on Amazon. If you have any additional questions, both Molly and Clarissa are food addiction professionals and work one-on-one with clients. You can find their websites and email addresses in the show notes. Be sure to tune in every Friday when our new episodes drop. As Vera loves to say, the power is ours.

4
0:37:41
when our new episodes drop. when our new episodes drop. As Vera loves to say, the power is ours.

Transcribed with Cockatoo