What to learn more about your genetic obesity risk and why understanding your methylation gene impact matters? Check out our audio transcription.
The genetic obesity risk & why methylation matters
Dawn (00:00):
Hello and welcome to the Gastric Health Show. My name is Dawn Boxell, and this week we are talking about your genetic obesity risk and why methylation matters. So some of you may be thinking, okay, I’m not even sure what methylation is, but I want to assure you. That you will understand fully once we complete this conversation. But really kind of just laying the foundation to truly understanding if you have obesity. Or you feel like you’re struggling with your weight, understanding your obesity risk is super empowering in allowing you to make informed decisions.
Dawn (00:52):
And when we look at genetics, we look at them in pathways because they all cross into each other’s areas. So you can’t just look at one gene and expect to make an educated decision on what that gene is going to do because it could be in other pathways. So methylation is one pathway that we look at when it comes to cellular systems.
Dawn (01:26):
So we’re going to kind of dig into this and hopefully give you a little bit of an insight that will help improve your understanding with methylation and why it even matters. Especially if you feel like you have a genetic obesity risk. So you may not have a genetic test to tell you this information, but your intuition or your gut tells you that maybe you have some of these obesity genes and maybe they’re a high impact.
Research shows that your genetics lay the foundation
Dawn (02:01):
And we’ll get into that so that you understand that better. But I think honestly, we can all agree that obesity is complex and multifactorial and unlikely driven by just one factor for most of us, right? So understanding your methylation efficiency combined with your genetic obesity risk is important. So that’s where we’re going. Research shows that your genetics lay the foundation, but the interplay between methylation, inflammation, detoxification, your glucose and insulin regulation, hormones, gut bacteria, all of those contribute to your difficulties in managing a healthy weight.
Dawn (02:50):
And unfortunately, healthcare sometimes oversimplifies the problem by focusing on really an ineffective calories in calories out model because that doesn’t work for every person. And I think if you’ve had bariatric surgery, you probably realize this more than any other population. So unfortunately, healthcare will sometimes look through the lens of weight bias and being a dismissive practitioner, just fully placing blame on the patient that you don’t have willpower and you have poor behaviors when in reality that is just not it.
Dawn (03:35):
And that practitioner may have a misunderstanding or just a delayed understanding on how genes work. So unfortunately, there has been kind of a delay in the scientific understanding that your genes are truly not your destiny. So just because you have obesity genes does not mean that you will become and have to stay obese. Consider that and remind yourself of that, that just because you have these genes doesn’t mean you can’t do anything about it because there are plenty of things you can do to help improve the situation that you’re in.
Dawn (04:24):
And I would say probably until recently. The role of genetics, epigenetics and the gut microbiome were really not fully understood. And it’s really been in the last couple of years that since I’ve taken a few courses, I have come to realize that many may have been misguided in their weight management approaches. So maybe offering only appetite suppressing medications or surgery as our only alternative to help treat obesity may have been misguide. So I do want to preface this by saying I 100% still believe in bariatric surgery and medications that can support weight loss and appetite regulation.
Just surgery and medications are not your only options
I am still for that, and I would say even more so when it comes to genetics. I think this just really opened my eyes to truly see the full picture and the full impact of why some people truly continue to struggle. So I’m hoping that I can plant this seed with you that you will explore this further because. I don’t want you to have this understanding that you can’t lose weight if you try it on your own or if you work on diet and lifestyle behaviors and focus on your genetics and those pathways that are mostly impacting you based on your genes.
Dawn (06:11):
I want you to understand that though, just surgery and medications are not your only options. So if you feel like, Hey, I’m struggling. I’ve had bariatric surgery, I’ve regained some, or maybe even all of my weight back, what has happened? It, a lot of patients will come and say, I feel like I’ve failed because they have regained and I’ve counseled thousands of patients who have lost their weight and kept it off. And then I’ve also counseled thousands of patients who have lost the weight and regained it all.
Dawn (06:47):
and sometimes even plus. So to me, as a practitioner and now understanding this full effect of genetics, I really see why those people who regained all or more or at least a good portion of what they lost, I understand why, and our approaches to deal with that have been poor. And it’s definitely not a 1200 calorie, 50 gram carb protocol that you’re supposed to follow, and I promise you it’s not.
Dawn (07:27):
So I want you to keep your ears open and an open mind with what I’m coming to you with because. I think this can hopefully lay a foundation that maybe you haven’t fully understood. I will say it truly has transformed how I practice and the focus that I really want to offer my patients and people in general because I want you to know that there are solutions and there are things we can do to set you up for long-term success that you get out of the diet culture cycle, and you truly focus on what works best for your body based on your genetics.
You have to find what works best for your body and your genetics
Dawn (08:13):
So really we understand that it’s all kind of new genetics, epigenetics, the gut microbiome, this is all new. So unless you’ve taken additional training, you don’t understand this yet. If you are a healthcare practitioner or you are visiting one frequently, if they don’t have this connection, it’s truly not their fault.
Dawn (08:40):
They just haven’t been expose to enough of it yet to have this understanding. So be patient and just consider working with people who have this knowledge so that you can be ahead of the game. But there are over 25 genes that influence weight loss, gain and maintenance, and certain gene variations that can make it harder to lose weight or maintain a healthy weight. So this is why a one size fits all approach just doesn’t work great when we just lump everybody into one diet protocol.
Dawn (09:21):
Like I was saying, 1200 calories, no more than 50 grams of carbs, exercise 300 minutes a week. I mean I, you have no idea how many practitioners have prescribed this to patients that I work with. Again, I’m not bashing that protocol in a way that it can’t work because absolutely it could work for some people, but this is not a protocol for mass populations to follow.
Dawn (09:55):
You have to find what works best for your body and your genetic makeup. So for example, your genes can affect how much and how frequently you eat, as well as how you experience hunger and fullness. So maybe this is part of the picture. Maybe if you find yourself gravitating towards certain foods or you can’t seem to stay out of the snacks, maybe this is part of your story and why you struggle, but having obesity genes does not necessarily mean that you will develop obesity.
Dawn (10:36):
So even though there are 25 plus genes that influence your hunger, your appetite, and how well you can even lose weight, it doesn’t mean that you are guarantee to have obesity even at all or for the rest of your life. So what I want you to understand is that there are actually genes that are protective and can improve your ability to fight against the disease.
Gene’s impact is crucial for effective weight management.
Dawn (11:09):
So understanding a gene’s impact is crucial for effective weight management. In fact, genetic impact is sorted out as protective, no impact, low impact, medium impact, high and very high. So all of those, your genes get ranked based on their impact. Just because you have those obesity genes doesn’t mean that they are going to have an impact that is going to prevent you from losing. So let’s kind of do an example. What if out of 25, weight and appetite regulation genes, 19 of them were either protective, no impact or low impact.
Dawn (12:02):
And I’ll kind of explain this. When I do do a genetic interpretation, I focus mostly on very high and high impact. Those are the ones that have the strongest impact for shifting your health. So those are my main impacts, but I’m also paying attention to your symptoms, your lab values, and your health goals.
Dawn (12:30):
So if I know, and I’ll just preface this and say that all of my bariatric patients. Or any patient who tells me that they have put on weight or they’re trying to lose weight. I focus several slides in my presentation to energy, and that is kind of how your body manages calories so that you truly understand these, the impact that these obesity genes and weight regulation genes and appetite regulation genes play a role in your health. So let’s assume that you have out of the 25, the influence that 19 were either protective, no impact or low impact.
Dawn (13:18):
So that only leaves six genes that are influencing your ability to regulate your weight and appetite. Six, not 16. And here’s the thing, depending on if some of those six could fall in the medium, which may or may not even be a concern. So I’m just wanting you to see that just because you have these genes, it does not mean that that is going, that gene is going to be express and you will experience it, nor does it mean that you can’t turn that gene off so that you can achieve weight loss.
Six genetic influence how well you can manage healthy weight
Dawn (14:01):
Okay, so now let’s get a little bit broader. So yes, you have those six genes influence how well you can manage healthy weight and would those six genes would interact with other higher impact genes. So again, we look at pathways and kind of the body systems, cellular pathways. We look at cardiovascular, we look at energy, which is your calories and weight and all that. We look at activity and exercise and we look at nutrients, so cellular systems, cardiovascular energy, activity, and nutrients.
Dawn (14:42):
So six different categories and each of them are kind of broken down into the different impact that your genes exhibit. So if these are going to impact with those higher impact genes that maybe are in these other categories. But what if your genetic roadmap showed the inflammation and glucose in insulin regulation had the highest impact, not weight, not energy, which would fall in the energy pathway. What if that was not the highest impact?
Dawn (15:22):
How would that make you feel? Would that make you feel a little bit more empowered that hey, maybe I can beat this. Maybe I do have options. And that’s what I want you to see. That you have options and you just have to know where to focus. So if it’s really your glucose and insulin that truly is driving it, or you just have so much inflammation going on. Or maybe it’s detoxification and your body does not detoxify well, and yes, you have liver and kidneys to do that and you can sweat, but just because you have that does not mean that all the chemical processes that are to occur at the right times mean doesn’t mean that that’s going to occur
Dawn (16:12):
because you might have deletions in some of your genes. Which is not uncommon if you had these six genes that influence weight and appetite regulation and were seeking weight loss, but it showed that the inflammation and glucose and insulin regulation and maybe even detoxification had a higher impact, focusing on lowering your inflammation, your blood sugar, your insulin and supporting your detoxification would be more impactful than a standard protocol of counting calories and following a restrictive diet while you exercised more correct or you followed that protocol.
Dawn (17:00):
I talked about 1200 calories, no more than 50 carbs and 300 minutes of exercise. That protocol that I hear prescribed frequently from other types of healthcare practitioners is not going to benefit. You in the way that you are thinking it’s going to help. As you can see, those who are overweight or obese may or may not have impactful weight in appetite regulating genes causing their issues. And this is why knowing your genetic roadmap can be a great guide to turn disease and obesity genes off. So again, I think it’s important to consider this if you are really struggling
Dawn (17:48):
With getting the weight off and maintaining it. Because this is just super informative in laying that foundation of taking you in the right direction that can support you better. So because of all of this over the next several weeks, we are going to break down the genetic pathways that are influential in contributing to weight and appetite regulation, that lead to app, that lead to obesity. And this week we are going to uncover the genetic obesity risk and why methylation matters.
The Methylation Pathway
Dawn (18:24):
First, the methylation pathway. So methylation is just a biochemical process that ensures that all cells within your body function optimally and methylation performs. Many functions including repairing genetic material, making energy, dealing with stress, handling inflammation, detoxifying cells, and regulating your brain chemistry. And it is also essential for turning genes off and on, which is critical for maintaining proper cell function. Now, what is the role of methylation in obesity and methylation is crucial. To the regulation of energy homeostasis and body weight.
Dawn (19:10):
So calorie balance, think of it that way. So instead of energy homeostasis, think of calorie balance and body weight. Several studies have reported differences in methylation patterns between lean. And obese individuals suggesting a link between epigenetic modifications and weight regulation. And in one study, researchers found that obese individuals had significantly higher levels of DNA methylation of the leptin gene than lean individuals.
The Role of Methylation in Obesity:
Dawn (19:42):
So adipose tissue produces leptin, which is a hormone that regulates your appetite. And energy expenditure and low leptin expression and increase appetite may be associate with high levels of meth methylation of the leptin gene. Then another study found that DNA methylation levels of the insulin receptor substrate one or IRS1 gene was significantly lower in obese individuals compare to lean individuals. In addition to its role in insulin signaling. IRS1 is also an important regulator of glucose metabolism.
Dawn (20:26):
important piece when it comes to weight management. It has also been shown that lower methylation levels of the IRS1 gene are associated with increased expression. And insulin sensitivity, which may protect against obesity and type two diabetes. So these studies suggest that the DNA methylation is crucial. Is crucial to regulating genes involved in energy homeostasis and body weight regulation and altered level of DNA methylation may contribute to obesity by altering gene expression.
Genetic Involved in DNA Methylation and Obesity:
Dawn (21:06):
Now, genes involved in DNA methylation and obesity. Several genes have been linked to the regulation of DNA methylation and the development of obesity. Again, keep reminding yourself that methylation is what turns the genes on and off. And plays a role in the behavior of your genes and metabolic processes. So again, this piece, the methylation piece is an indirect connection. So if methylation is a very high impact and you’re not supporting it well. With diet, lifestyle, those types of things, or even some supplements because you can’t support, and I’ll get into it in a minute, but some of the B vitamins are directly connected to this methylation pathway.
Dawn (22:08):
So if you aren’t taking the right supplements, there’s no medication that’s going to do this. It is a supplement that is going to help. You can’t, it’s not a prescription. This is something that you can buy over the counter get online that is going to support your methylation, and you will understand a little bit more in a minute. But several genes have been linked to the regulation of DNA n methylation and the development of obesity.
Dawn (22:36):
One of the most studied genes is the PPARY gene, and this gene plays an important role in adiposity differentiation and lip in lipid metabolism. So think of fat cells and how your body metabolizes fats. So a study found that methylation levels of the PPARY gene were significantly higher in adipose tissue from obese people than in lean individuals. And higher methylation levels were associated with lower PPARY expression. And impaired lipid metabolism resulting in obesity and metabolic disorders.
Dawn (23:20):
Then the MC4R and I’ve talked about this gene before, has also been linked to DNA n a methylation and obesity. It plays a critical role in appetite control in energy homeostasis. And a study found that methylation levels of the MC4R gene were significantly lower in obese individuals compared to lean. And a decreased methylation level was associated with increased MC4R expression and energy expenditure, which may contribute to obesity prevention.
Dawn (23:55):
And these studies suggest that DNA methylation of key genes involved in energy or calorie balance. And body weight regulation could contribute to the development of obesity. So next is DNA methylation and adiposity or fat cells. Think of adiposity as your fat cells. So adiposity and fat distribution are also associated with DNA methylation. A person’s adiposity refers to how much fat they have while fat distribution refers to how it is distributed on their body. And think about the different body shapes, somebody’s a pear shape or an apple shape, that type of thing.
We all carry our weight in different areas
Dawn (24:41):
So we all carry our weight in different areas that some, it’s easier to hide than others. At a glance, some people don’t seem like they really carry their weight bad. Whereas other people, they carry it in a way that is not easy to hide and not easy to mask. So on the flip side, some certain body shapes have higher health implications. That just means that you might have a higher disease risk because of where you carry your fat.
Dawn (25:19):
and it’s just harder on your organs when it’s carried, especially in your midsection. At one point they had considered switching away from BMI and doing a waste circumference. And I remember that years and years ago that they were contemplating shifting to this. And I remember thinking, oh my gosh, all of Americans are going to fall in this category because of the numbers that they were giving.
Dawn (25:45):
And I was like, oh my gosh, this is awful. We’re going to have an awful time managing this waste circumference expectation that people are supposed to achieve. And I’m like, Ooh, that seems scary. Luckily it never passed. But I do know that it is something that practitioners look at, and it is something to consider because it does come with health implications. The more you have around your midsection, the higher your health risks are.
Dawn (26:15):
So the DNA methylation patterns of lean and obese individuals differ suggesting a link between epigenetic modifications and obesity. In a study found that obese individuals had significantly higher levels of DNA methylation of the leptin gene. Which regulates appetite and energy expenditure in adipose tissue. So graylin is our hunger, hun hormone and leptin is our fullness or satiety hor hormone.
Dawn (26:44):
And higher methylation levels were associated with lower leptin expression and increased appetite. Which could contribute to the development of obesity. Studies have also investigated the relationship between DNA methylation and fat distribution. According to a study visceral adiposity or just the fat cells that are around your organs, which just as a side note is that during the transition to menopause, you naturally start storing more fat around your organs. So you have to work harder to prevent that and to remove that.
DNA methylation and adiposity
Dawn (27:35):
So the visceral adiposity, the accumulation of fat around the internal organs is associated with DNA methylation levels of the adiponectin gene. Which regulates glucose and lipid metabolism. The more fat cells you have around your organs or this visceral adiposity. This is going to influence your glucose and lipid metabolism. Again, as you transition into these different stages of life, think mid to late forties into fifties and sixties, you are transitioning through this at your highest peak. This is when your body is kind of working against you and gravitating towards storing fat in these areas.
Dawn (28:28):
And I will say it, it’s been, I will say it’s been a theory that for females as your estrogen drops usually because our fat cells can make more estrogen. So as you lower your estrogen level, your fat cells can produce estrogen. And that’s kind of the theory that why during menopause, we start packing on the pounds so that our fat cells can provide a source of estrogen for us to support us in a better way. But it kind of negates some of the benefits because as you start packing on the pounds.
Dawn (29:13):
it’s kind of like now the benefits are gone because now I’ve gained 20 pounds. And it’s no longer benefiting me and I’m not getting enough estrogen just from the fat cells. So it’s not a great strategy, but it is an interesting theory to think about. So, but in the presence of higher methylation levels of the adiponectin gene. There was lower adiponectin expression, an increased visceral obesity, which increases the risk of metabolic diseases like type two diabetes.
Genetic Variations and Methylation
Dawn (29:49):
And according to these studies, the DNA methylation regulates adiposity or fat storing and fat distribution genes. And dysregulation of DNA methylation patterns could also alter gene expression and contribute to obesity and related metabolic disorders. So again, you want your methylation pathway efficient. You want, if you have high methylation or high or very high impact methylation genes that makes you, makes your methylation inefficient, you would want to be very supportive in optimizing methylation.
Dawn (30:36):
That has to be something that you consider because you are going to not be able to turn off those obesity genes. You’re not going to be able to turn on those healthy type of genes that would support you better. So let’s talk about gene variations and methylation. Genetic variations or mutations in genes involved in the methylation pathway can affect methylation patterns and consequently metabolic function. Just like we’re saying, all of this matters because remember, methylation controls the behavior of genes and metabolic functions.
Dawn (31:17):
So you want this working efficiently, you want this smooth, you want this working well. So very popular gene that’s in the methylation pathway. In the methylation cycle is MTHFR and the MTHFR gene and folate metabolism is probably one that. There’s probably a lot of people that know if they have this genetic mutation, if they have one or both of them because there are two of them.
MTHFR Gene and Folate Metabolism
Dawn (31:52):
But the MTHFR gene is one of the genetic variations that affect methylation. It encodes the enzyme that is essential for folate metabolism. And you think, how would that matter? Who would really care about folate metabolism? Well, if you’ve had bariatric surgery and you’ve had a low folate level or a low B12 level. You may be needing to approach it in a different way because you’re just. Any strategy will not work on hitting those that methylation cycle appropriately.
Dawn (32:27):
So the B vitamin folate is crucial for DNA methylation and mutations in the mtf MTHFR gene can impair folate metabolism and alter methylation patterns. So if you have a low folate level, then you are not going to methylate. Well, this in turn can lead to metabolic disorders such as obesity. The MTHFR mutations are associates with obesity, insulin resistance, and other metabolic disorders in individuals. And according to a study, individuals with a particular mutation in the MTHFR gene, this is the 677 T gene. So this is the snp.
Dawn (33:13):
The CEX seven seven had a higher risk of developing obesity and insulin resistance than those without this mutation. And it’s not uncommon for individuals to have the 1298. So there’s an MTHFR 677 and a 1298. So those two genes, you can have one or both. If you have both, that means you’re homozygous.
Dawn (33:38):
And that means that both of your parents gave you this so you can thank them both. It wasn’t just one of them. So both of them gave you this MTHFR genetic mutation. And just a side note is when you have both of those. You are definitely at a higher risk for depression. So if you struggle with depression, you really need to make sure you understand if you have these genetic mutations and making sure that we’re supporting your methylation pathways better, more optimally, especially your folate, especially your b12,
Dawn (34:16):
especially your B six, because all of those play a role in the methylation. Now, other genetic variations of methylation, so in addition to the MTHFR gene, a lot of these are not going to be familiar for a lot of you, but they’re important to understand. And if you do a genetic test with me, you would know all of these.
Dawn (34:37):
You would learn all of these different genetic variations, and it can help support your journey to health. So these include BHMT and the BHMT enzyme is involve in the metabolism of homocystine. And according to a study, methylation levels of the BHMT gene were associated with elevated body mass index. Or BMI in children indicating that epigenetic modifications may contribute to obesity. The next one is CBS, and CBS is an enzyme that plays a role in methionine metabolism.
DNA methylation of the CBS gene
Dawn (35:18):
And according to a study, children with higher levels of the DNA methylation of the CBS gene had greater BMIs suggesting epigenetic modification to this gene contribute to obesity. So both of these are kind of saying the same thing, comped COMT. This comped enzyme plays a role in the metabolism of catecholamines such as dopamine, epinephrine, and nore epinephrine.
Dawn (35:45):
A study published in molecular psychiatry found that DNA methylation levels of the comped gene were associated with BMI and. Body fat percentage in women, higher methylation level levels were associated with increased BMI and body fat percentages. So this comp gene also kind of influences your detoxification in your liver so it can slow down or speed up that detoxification. So this is definitely something that we pay attention to.
Dawn (36:21):
The next one is MTHFD1, and this is an enzyme involved in folate metabolism. So this kind of goes with the MTHFR. It just is not as popular as the MTHFR that was discovered decades ago. But according to a study, higher DNA methylation levels of MTHFD1 gene. Were associated with increased BMI and adiposity in women. And the MTHFR also plays a role in folate metabolism.
Dawn (36:51):
If we recall, we talked about that the two common polymorphisms of MTHFR gene are the 1298 in the 677. Like I had mentioned, and they have been linked to obesity and related metabolic disorders. And additionally, methylation patterns of the MTHFR gene have been associated with obesity and related metabolic diseases. The next is MTR and this MTR is involved in methionine metabolism In a study published in the Journal of Nutri Genetics. And Nutrigenomics found that d n methylation levels of the MTR gene were associated with BMI and waist circumference in women.
Dawn (37:33):
And higher methylation levels were associated with an increased BMI and waist circumference. So you have to pay attention to is this MTR contributing? Is this contributing? Is it a high impact gene in your genetic results? The next is MTRR. So there’s MTR and MTRR and MTRR is an enzyme that plays a role in methyonine metabolism as well.
MTRR DNA methylation
Dawn (38:02):
And they found that MTRR DNA methylation levels in women were associates with their BMI and adiposity. The next one is NBPF3 and it is a gene that has been, I implicate in neural development study found that higher methylation levels of the NBPF3 gene are associated with increase of BMI and adiposity in children. Next is NQO1 and it is involved in detoxification. And a study reported in the Journal of Clinical Endocrinology and Metabolism found that DNA methylation levels of the NQO1 gene were associated with BMI and insulin resistance in men.
Dawn (38:49):
And the study suggests that higher methylation levels were associated with bmi with increased BMI and insulin resistance. And we’re, we’re getting close to the end here. But the next one is OGG1 and this is an enzyme that is essential for DNA repair. And a study found that the DNA methylation levels of OGG1 gene were associated with BMI. And adiposity in women and researchers found that the higher the level methylation levels were associated with increased BMI and adiposity. The next is PEMT, and this plays a role in phospho lipid. This plays a role in phospho lipid metabolism.
Dawn (39:32):
In a study published in the Journal of Clinical Endocrinology and Metabolism dna. Methylation levels of PEMT gene is link to BMI and adiposity in women. A higher methylation level was associated with higher BMI and adiposity. The last one is TCN2 and it is a protein that plays a role in the transport of B12 or vitamin b12. And in a study published in Nutrigenetics and Nutrigenomics DNA methylation levels of the TCN2 gene. Are associates with BMI and waist circumference in women.
Dawn (40:10):
It was suggested that BMI and waist circumference increase with higher methylation levels. Studies show that mutations in these genes have can affect methylation patterns and increase the risk of metabolic disorders. And researchers have found that individuals with a mutation in the MTRR gene have lower levels of DNA methylation. And a higher risk of metabolic syndrome. So implications, what are the implications for the treatment and prevention of obesity?
DNA methylation in the development of obesity
Dawn (40:43):
The discovery of the role of DNA methylation in the development of obesity has significant implication for the treatment and prevention. And it’s becoming increasingly clear that epigenetic changes are biomarkers for obesity and metabolic disorders. Methylation is the process involve in actually turning genes on or off. And if we optimize our methylation, we can reduce our risk of developing certain diseases and cancers. According to a study, the DNA methylation levels of the FTO gene. Which is the very first obesity gene that was discover, can predict obesity and type two diabetes.
Dawn (41:26):
In addition, targeting DNA methylation could provide a potential therapeutic approach for the treatment of obesity. A number of studies have examined how dietary interventions can affect DNA N a methylation patterns in obese individuals. According to a study, a higher fiber diet can alter DNA methylation patterns in genes involved in lipid metabolism. And calorie balance in obese individuals potentially improving their metabolic health. So when we tell you we want you to eat more fiber. This is one reason a number of potential treatments for obesity and relate to metabolic disorders are currently being investigating.
Dawn (42:10):
That target DNA methylation in a study published in diabetes dna, N a methyl transferase inhibitor treatment. Improved insulin sensitivity and glucose metabolism. And obese mice suggesting that targeting DNA n a methylation could be a promising way to treat obesity. So let’s wrap this up. DNA methylation plays a critical role in the regulation of energy homeostasis and body weight. And dysregulation of DNA Methylation patterns might contribute to obesity and other metabolic disorders.
Implications for the Treatment and Prevention of genetic Obesity:
Dawn (42:45):
Increasing our understanding of the epigenetic mechanisms involved in the regulation of body weight. May provide us with new insights into the development of obesity and aid in the development of new prevention and treatment strategies. And in spite of the need for more research in this field. The potential implications of DNA methylation for the prevention and treatment of obesity are promising. So again, I think if you just take a pause and look at the big picture of if we optimize your body systems and
Dawn (43:22):
we work on making sure that these genes that aren’t functioning efficiently start functioning efficiently. That can support your body in a way that maybe you have never had. If you, for one, if you’ve never had your genetics tested. You may not know you have this genetic mutation of MTHFR that. So many people more than I think 40 or 50% of the population carry this mutation and some. I don’t know what the percentage is that carry both mutations.
Dawn (44:01):
So again, is this part of your story that you are fully unaware of. So that’s where the genetic piece can really help give you the roadmap that you need to really map out where to go next. If you were super tired of trying a bunch of different diets that end in the same place where you are struggling. I would highly encourage you to first check out our gastric health membership because. That’s where you’re going to get the best value for any testing.
Dawn (44:36):
So you are welcome to buy the testing outright and work with me through that. And we’ll do that for a few months and you would be done, or you could do the. Become a gastric health member, which there’s no contract, so you can end at any time with the membership. But it allows you to get 40% off of the genetic testing and work with me through the protocols. And you just continue that membership as you need it.
Conclusion:
So if you find that after we’re done, we’re working in three months. Or we’re done working in six months through the protocols and getting you to the goals to accomplish the goals you want. You can edit at any time or you can kind of just keep going. keep it ongoing so that you have the support if something arises. So regardless, I’d encourage you to check out our membership because. It’s truly the best value to get one the information that you need, the support and coaching that. You need so that you know how to address your health.
Dawn (45:45):
So I hope you guys have enjoyed this. I get super excited about the genetic piece and understanding the obesity risk that comes with the bariatric population. If you are considering doing a genetic test, just reach out to me because. I can send you a sample report so you can kind of see what it looks like and see if this is for you. But I’m telling you, you will not be disappoint To date, I have never had a report that I have interpreted that I couldn’t have told you. What your health has been like and what you’re currently struggling with. It has a hundred percent of the time. And even me personally, it a hundred percent told me exactly what my life has been like and what I have struggled with and. When those genes got turn on, how and why I was struggling.
Dawn (46:42):
So it is an awesome tool. So if you’re considering it, reach out to me. I’d be happy to share any type of information, a sample report, or just more information on it. I’d be happy to chat about that if needed. But you guys have a great week and we will see you next time. Bye-bye.
Listen, Learn, Enjoy…
References & Links:
- Li, F., Feng, Q., Lee, C., Wang, S., Pelleymounter, L. L., Moon, I., … & Weinshilboum, R. M. (2008). Human betaine-homocysteine methyltransferase (BHMT) and BHMT2: common gene sequence variation and functional characterization. Molecular genetics and metabolism, 94(3), 326-335.
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