Metabolic liver health: how to assess risk, catch dysfunction early, and more (AMA 88 sneak peek)

Key Takeaway

Stop drinking your calories today—especially sugar-sweetened beverages. The episode’s clearest practical advice is that liquid carbohydrate calories, particularly fructose-containing drinks, are easy to overconsume, provide little satiety, and can increase liver fat production. Replace soda, juice, sweetened coffee drinks, and energy drinks with water, sparkling water, or unsweetened options. This single change can reduce overall calorie intake while lowering a major metabolic burden on the liver.

Episode Overview

Peter Attia explains why the liver is a central indicator of whole-body metabolic health, not merely an organ affected by alcohol. He traces the progression from metabolic stress to liver fat, inflammation, fibrosis, and cirrhosis; discusses visceral fat, muscle mass, fructose, alcohol, and genetic risk; and emphasizes that prevention should focus on the person’s overall metabolic phenotype.

Full Transcript

Transcript of Metabolic liver health: how to assess risk, catch dysfunction early, and more (AMA 88 sneak peek) from The Peter Attia Drive Podcast. Auto-generated from episode audio; may contain minor errors.

Hello everyone, welcome to the Drive podcast. I'm your host, Peter Aya. Peter, welcome to another AMA. How are you doing? Very good, thank you. Perfectly. So, today we're doing an entire episode on one topic, which is: the liver and metabolism. In the past, you have called the liver, quote, the canary in the coal mine for metabolic dysfunction. So, I think it would be helpful to start with what you mean by that and why you think the liver is so important. Well, the liver is at the center of systemic metabolism for every macronutrient: glucose, fat, protein, and also cholesterol.

And by the way, let's not forget about ethanol or alcohol. So it's also one of the first places where stress arises and is responded to from anywhere in the system. If triglyceride levels in the blood are high, the liver intervenes. If glucose regulation deteriorates , the liver intervenes . If APOB or LDL cholesterol levels increase, the liver produces these particles. And the reverse is also true. If we look at the liver and see that it is under stress, we know that these metabolic systems are also under stress.

It's a two-way mirror between systemic metabolic health and what's happening in the liver. And that's why I think less about liver disease as a separate organ problem. Hmm, liver dysfunction is more of a parallel expression of systemic metabolic dysfunction. The leading cause of death in people with liver disease is not liver failure. These are cardiovascular diseases. Because the liver under metabolic stress overproduces particles containing apolipoproteins and increases insulin resistance , leading to atherosclerosis throughout the body. And so, um, it's a metabolic episode as well as a hepatic one.

Uh, and I think we should also mention this right away, when we talk about fatty liver disease, we're talking about a disorder that's estimated to affect over 38% of the adult population worldwide. Uh, that's hard to believe. Uh , this isn't something that happens to some unfortunate person you'll never meet. Uh, it will happen to almost anyone in the developed world who doesn't pay attention to it . And I think it's worth talking about what the liver does beforehand, right? So I think a lot of people, when they think about the liver, they usually think about processing alcohol.

So before we dive into metabolic diseases, can you outline a little more in detail what the liver does in the body? Of course. Hmm, and you're right , the alcohol structure dominates. Hmm, and it's a bit veiled. Hmm, as our previous guest, uh, Julia Waterrell, says, the liver has over 300 functions. Hmm, that's pretty impressive. Obviously, we won't be talking about many of them today. Hmm, but I find it helpful to conceptualize all of these functions as falling into four main categories. So, the first is detoxification.

The liver breaks down alcohol just as it breaks down almost any toxin that enters the body from food, drink, pharmaceuticals, inhalation, any toxin that enters the bloodstream , the liver plays a central role in its purification. Secondly, it is an immune organ. So, the first place where blood goes from the intestines is the liver . All blood from the intestines returns back into the portal system to the liver. So it is one of the first to respond to the entry of toxins or the leakage of bacteria from the intestines.

The third place is protein processing and secretion. The liver is the site of synthesis of many of the most common proteins in our blood, such as albumin, and such vital ones as blood clotting and platelet stimulation factors, apolipolyses, and peptide hormones such as insulinogenic growth factor-1 (IGF-1). The fourth category is where we will spend most of our time today, and that is energy exchange. The liver plays a central role in the absorption and synthesis of circulating fats and cholesterol and is one of the most important organs, if not the most important organ, for balancing blood sugar levels.

It's, you know, you can think of it as the metabolic center of the body, so when it's damaged, the damage isn't just limited to the organ itself. So, you mentioned the liver and blood sugar. Can you tell us more about the liver's connection to blood sugar control? Yes, it sounds simple, but the precision required to regulate blood sugar levels is extraordinary. Uh, and it never ceases to amaze me. This is one of my favorite things to explain to a patient. After eating, uh , glucose levels rise.

The pancreas secretes insulin, and insulin tells the liver to absorb glucose and store it as glycogen. So when you fast for a period of time and your glucose levels drop, your insulin drops, and then the liver does the opposite. It breaks down glycogen back down and releases glucose into the bloodstream. And when glucose levels are very low, it can simply produce glucose on its own. So, you know, if you don't eat for more than a day, the liver turns into a glucose-producing organ. If there is too much sugar to store as glycogen, the liver converts it into triglycerides, packages it into αPA- lipoproteins, um, and excretes them.

So I want people to appreciate the scale of this. So everyone, you know , think about the fact that you go to the doctor, they give you blood, and this , you know, is a fasting blood draw, right? And you get a number. Let's say this number you get is 90 milligrams per deciliter. This was your blood glucose level that morning when you came to the lab. If that's the case, your entire bloodstream at that moment only contained about 4.5 grams of glucose. That's about a teaspoon, not a tablespoon, just a teaspoon.

However, one meal, especially if it's a meal I eat, can contain many times that much, easily 90 grams of glucose, right? So 20 times more in one meal. And yet, despite this, a healthy person rarely exceeds the baseline level by more than a teaspoon. Right? In fact, I'm trying to think back to all the times I've worn a continuous glucose monitor, if I've ever seen a blood glucose level that was higher than about 160 milligrams per deciliter. A person with type 2 diabetes would rarely exceed one and a half teaspoons on an empty stomach.

And when we can go hours without eating, our glucose levels still stay in this range. In fact, if you don't eat for a few days, it can drop to, say, only 50 mg per deciliter. This is a monumental homeostatic achievement. And it's this reserve ability to titrate glucose in such small amounts that is the reason why early dysfunction is so easy to miss, and that's something that we, I will definitely talk about. Yes. So let's delve into metabolic diseases and how they affect the liver. And when you look at this, is there a structure that you typically use when discussing it with patients, explaining it?

So, I think the most useful framework is to look at metabolic liver disease , which goes through four stages. So, in the first stage, the liver is in metabolic stress . Hmm, and then in the second stage, in response to that, it starts to store excess energy as fat, and that's a condition known as steatosis. And then the third stage is, uh, steatosis, and that's just a fancy term for excess fat accumulating in the liver; This leads to inflammation of the liver, and then the liver begins to damage itself.

And then the fourth stage is the response to this damage, where scar tissue begins to form, and this is a term that people have probably heard, liver fibrosis. So these first three stages are, uh, largely reversible. It's with fibrosis, hmm, things are a little more complicated. Hmm, it is biologically reversible to varying degrees, especially if detected at a very early stage, but once the scarring accumulates to the point where the architecture of the liver is disrupted, that's when it becomes irreversible. The presence of fibrosis is what predicts the outcomes we usually worry about, especially cardiovascular disease , cancer, and even liver-related mortality.

So as we go through this exercise, I will keep pointing out where we are on this four-step diagram. And you said earlier that chronic caloric excess is a major factor in metabolic dysfunction. So can you walk us through the chain of events from excess calories to, ultimately, liver damage? Yes, it all starts relatively simply. If you consume more calories than you consistently burn, the body has to store this excess energy somewhere, and the liver converts most of it into triglycerides through the process of denovolipogenesis. It packages them into these particles containing apolipomeric amino acids (APO), namely VLDL and LDL, and transports them to adipocyte tissues for long-term storage .

And again, this is a normal, healthy physiological response . If we didn't have that ability, we would n't be here today. You and I wouldn't be talking to each other. Our species would have become extinct because we had to be able to store energy when energy was abundant, and we had to be able to draw on it when energy was scarce. So, for now, it's okay. Obviously, as you can see, at some point this will become abnormal. So imagine a fat cell as a warehouse. Hmm, they will accept every batch for a while.

Hmm, but as they gradually become overcrowded, they stop responding normally to insulin, which is the most important hormone involved in this process. And one of the molecular hallmarks of this process is the accumulation of a lipid intermediate called dasalog glycerol or DAG or DAG, which interrupts insulin signaling. So once this happens, the storage starts to malfunction. Instead of simply storing fat, these particular fat cells, or adipocytes, begin to release fatty acids back into the bloodstream. Exactly what you don't need if you don't intend to use them immediately.

The problem is that there is already too much energy in the bloodstream. So the last place you need more triglycerides is being released back into the bloodstream. So now the liver has to deal not only with the excess calories coming from food, but also with the excess fat that is being returned to the bloodstream from these defective fat cells. And what happens to free fatty acids in the blood? So the liver takes these fatty acids, as well as fats from our diet, because one of its main tasks is energy balance.

Hmm, but ultimately the same process is unfolding here. So lipid intermediates begin to accumulate. Insulin signaling is disrupted, and the liver becomes insulin resistant . People might remember the podcast we did with Ralph Defrono on this topic, and it was one of my favorite podcasts in the last year or two because it's just a master class on all the different types of insulin resistance and insulin resistance in muscle versus fat cells versus pancreas versus liver. They all look a little different. I'm not going to go into that right now, but if anyone wants to refresh their knowledge, we'll go over here and reference it in the podcast.

But here's the part that's really important. Insulin usually tells the liver to do two things. Stop the release of glucose into the blood and stop the formation of new fat cells. Why? Because if your insulin levels are high, you just ate. And if you eat , you don't need to inject glucose into your blood or create new fat. But when insulin resistance develops , the first signal disappears before the second. So, the liver continues to release glucose even when blood sugar levels are already high, while the pancreas responds by producing more insulin, which still stimulates fat production.

This is called selective hepatic insulin resistance , and it is one of the defining features of metabolic diseases. Initially, the liver exports these triglycerides in the form of particles containing apolipoproteins , and again, this means only LDL and VLDL, so dyslipidemia always accompanies this, and eventually production exceeds export. So, fat accumulates inside the liver, and now we have reached the second stage of our little linear progression. This is now steatosis. So what liver diseases are you concerned about as a result of this metabolic dysfunction? Well, the name was recently changed to reference the cause of the disease and to drop the fat in the name.

Hmm, because fat is essentially the end result of excess calories, but that excess is usually not fat itself. So excess calories often come in the form of anything. These can be carbohydrates, glucose, fructose. So, we used to call this disease NAFOLD, nonalcoholic fatty liver disease, and if it progressed to the inflammatory stage, it was NASH, which simply stood for nonalcoholic steatohepatitis. By the way , the NA in both cases, non-alcoholic, means just so we can try to understand that it was caused more by excess energy rather than damage caused by the alcohol itself, because you can also get alcoholic fatty liver disease and alcoholic steatohepatitis.

Um, okay. These things are called mazeld, m-asld, and mash, not TV shows. What does this mean? This stands for metabolic dysfunction associated with stomatic liver disease and statohepatitis. So, essentially, it's the same disease, just new names. And I apologize in advance. I will sometimes still call them naffy and nash, as opposed to masled and mash. Again, I apologize in advance for this, but please understand that this is simply a new nomenclature to try to more accurately reflect the disease process. And regarding this, so once the fat accumulates, is that the point where the liver starts to suffer real damage?

Well, that's a giant warning sign. This is not liver damage yet, but you are already on the path to liver damage. So imagine it as a liver shoving excess energy reserves into the manager's office because the shelves are full. Uh, something is clearly wrong, but nothing is breaking at the packaging plant yet . If this analogy helps, maybe it doesn't. The diagnosis of Masle D. is made when this steatosis is accompanied by another cardiometabolic risk factor, such as hypertension, er, prediabetes as determined by hemoglobin A1C, or even just type 2 diabetes, dyslipidemia, elevated BMI, or obesity.

Uh, again , these are just indicators for the poor, but you get the idea, right? So, fat in the liver accompanied by some other metabolic dysfunction is what we're looking for, and that's our second stage: both metabolic stress and fat in the liver. The real damage begins when this fat load causes inflammation. Um, hepatocytes, overloaded beyond their limit, actually start to die. Hepatocytes are simply the cells that make up the liver. Their death attracts immune cells, which release inflammatory signals that spread to neighboring cells. And it's this inflammation that, um, starts to shut down insulin signaling through a second separate pathway.

So resistance is now coming from two directions at once. Um, with even more insulin resistance, the neighboring cells now accumulate more fat and die as well. And then you get a wave of propagation, where each cell death leads to the next. So, as you can see, it becomes a kind of reinforced direct action loop. This transition from fat accumulation to active inflammation is the transition from stage two to stage three , which we call mASH ( Magnetic Anemia Disrupting Metabolism ). And the liver responds to dying cells just like any tissue.

It forms scar tissue. This is called fibrosis . This is our final stage of reflection on metabolic liver disease . As fibrosis accumulates, the liver moves toward cirrhosis. This is the final stage of scarring, when so much functioning tissue is replaced that the liver can no longer even perform its function. And you should remember all those other things I talked about about protein production, blood clotting factors, and detoxification. All this is starting to disappear. This is where the risk of cancer begins to increase dramatically. Fibrosis is where the truly persistent clinical risk lies.

And when we talk about metabolic dysfunction, we often hear about visceral fat as well. So what do we know about visceral fat and the liver? Does visceral fat specifically affect the liver? Yes, this is one of the most important risk factors for the liver. Not all fat is of equal importance or metabolically, um. Fat that accumulates around your organs is actually more prone to releasing fatty acids even early in the process. But the bigger factor is definitely location. So visceral fat, um, the fat around the abdominal organs, goes directly into the portal vein, which is one of the two sources of blood supply to the liver.

Um, this is the one that drains the gastrointestinal tract. So, the whole gut and all the, um, metabolites that come from digestion. So subcutaneous fat, um, releases fatty acids that initially diffuse throughout the bloodstream. So, it is much less concentrated when it comes to injection directly into the liver. Visceral fat bypasses all of this. And that's the difference between, you know, when someone is yelling at you from across the house, and when someone is yelling right in your ear. Same signal, hmm, but much higher intensity because of where it's coming from.

And the data confirms this. Consequently, in one cohort, visceral fat area assessable by CT predicted steatosis independently of BMI and liver enzymes. So, patients with a visceral fat area of more than 200 cm² had a 7.5- fold increase in liver steatosis compared to people with a body area of less than 100 cm². And if you look at the NHANES database among people diagnosed with mass D, the all- cause mortality rate (in the top quartile) of visceral atypism was almost three and a half times higher than in the bottom quartile.

So, visceral fat predicts liver pathology, and in people who already have liver disease , visceral fat predicts a significantly higher risk of death. And in the past, when talking about metabolic health, you often talked about the importance of strength training. So what do we know about how strength training interacts with the liver's role in metabolic dysfunction? Well, even more than the liver, skeletal muscle is the main glucose sink in the body. In fact, it is by far the largest glucose absorber in the body. So they pull blood sugar from the bloodstream and store it as glycogen.

So about 3/4 of your total glucose storage capacity is in your muscles, and about a quarter is in your liver. Hmm, and this is again storing it in the form of glycogen. So what does less muscle mean? So, this means a lower ability to buffer glucose . So more of this burden falls on your liver. Hmm, that's why you see metabolic liver disease in people who actually have a normal BMI but have very low muscle mass. Hmm, sarcopenic obesity is the technical term for this, or what people call "skin fat," and numerous longitudinal cohort studies indicate the same thing.

More muscle predicts both fewer new cases of liver disease and higher recovery rates. The most impressive figure, uh, comes from a large 7- year Korean cohort. People who gained the most muscle during the study resolved their breast problems more than four times more often than those who gained the least. We'll include all of this in the show notes. So, whether it's prevention or the reverse, the direction here is pretty clear, so strength training is something that is essential if you're trying to address the problem of metabolic dysfunction.

And do we know anything about whether fructose can be more harmful than glucose? This is a very interesting question, and it is very easy to get confused about it. Hmm, the purest human experiment. Hmm, and I want to focus only on human experiments, because you could spend all day on this issue, Nick, if we wanted to talk about everything animal-related. But, uh, the purest human experiment is a randomized study of 94 healthy men who consumed moderate amounts of fructose ( gm), which is again pure sweetener (gm), and antimeric sucrose (a 50/50 mix of fructose and glucose ) or glucose-sweetened beverages (gm), for seven weeks at a stable weight.

So it's very important when you're doing these studies to keep the subject's weight stable, because if you don't, it's going to mess everything up. In this study, fructose and sucrose approximately doubled the baseline mechanism for fat production in the liver. This is the so- called denovo lipogenesis pathway. Denovo simply means new , and lipogenesis means the creation of fat. While glucose did not do this. So, at least in this study, fructose may behave differently than glucose in the human liver. And where this is most clearly manifested is in these dimensions of denovo lipogenesis.

But for the more complex outcome, actual steatosis, controlled feeding studies show that the dominant factor is excess calories, not fructose itself. So if you replace fructose isocaloricly with other carbohydrates, the fat in the liver hardly moves. So, calorie for calorie, the honest signal regarding fructose is directed towards lipogenesis, which is an intermediate indicator , but not the end result. Fructose has earned its reputation in the form in which it comes. For example, liquid sugar in soda or other drinks with high fructose corn syrup , which are very caloric, do not cause feelings of satiety and are easy to consume, and cohort data does link sugar-sweetened beverages to a higher risk of edema or risk of obesity.

So the practical advice is that reducing your intake of sugar-sweetened beverages is one of the most effective dietary steps for people with insulin resistance or liver disease. But really the main reason for this is that it will have a further impact on reducing calorie intake. So, one of the things that I would definitely advise people with fatty liver disease is not to drink calories at all , and especially not to drink carbohydrate calories, and especially not to drink calories that contain fructose. There is much that is special about this statement.

It sounds like it was extremely important. Hmm, okay. So, let's go back to what we were talking about earlier, which is that when people think of the liver, they think of alcohol. So, how should we think about alcohol in relation to the liver? Yes, alcohol is a fairly clean story. You remember a second ago I said that the reason we should put soft drinks, you know, whatever , in front of them is to differentiate them. Hmm , they can cause fatty liver disease on their own.

So, alcohol-associated liver disease , which, by the way, happens more often than we think. It's very easy to focus only on metabolic versions of soft drinks. But if you actually look at the people who need liver transplants, um, I don't remember the latest numbers, but the last time I looked, I was really surprised by how many, I think, more of them came from drinking alcohol than from drinking soft drinks. Again, I could be wrong, but I just remember being kind of surprised. Hmm, given that, it works through a different mechanism than excess calories, but it turns out the result is pretty much the same.

You go through these categories of steatosis, insulin resistance , fibrosis, and eventually cirrhosis. Uh, a different mechanism, um, so it's very harmful if you combine it with metabolic dysfunction, as is often the case. So now you get essentially a two-pronged synergistic attack when you have a calorie surplus and alcohol consumption at the same time . The combination of metabolic dysfunction and alcohol consumption has recently gotten its own name, and frankly, I think we're a little ahead of ourselves, namely metabolic- alcoholic liver disease or metal-related liver disease.

I will never do this again. There is a very revealing cohort study from the NHANES database in patients with existing cardiometabolic risk factors. If you already had a risk factor, steatosis itself was not associated with increased all- cause mortality. But steatosis plus what they described as moderate, and I would call moderate, plus alcohol consumption resulted in hazard ratios of 1.4 for all-cause mortality, 2.35 for cancer mortality, and a whopping 15, please check that number again. Yes, 15-fold for liver-related mortality compared to people without steatosis liver disease.

So to translate that into actual relative risks, well, the cause of death from anything went up by 40% . Cancer mortality increased by 135%. And mortality from specific liver diseases increased by 1400%. So again, the point of me saying this is not to tell you to never drink again. This is to explain that when you add alcohol to liver disease , things get really bad. Now, if we look at the pattern of alcohol consumption, hmm, there may be something to learn here again. So, acetal aldehyde is the main driving force behind alcohol's damage to the liver, and it builds up faster the more you exceed about one drink per hour.

So mechanically I get asked this question all the time , but I think it's safe to say that seven drinks in one evening is probably worse for you than one drink in a night. Seven , you know, nights in a row. Hmm, again , I haven't seen data on this, but when you understand the mechanism of action, I think it makes sense. Um, but I think the point is, you know, there's no human data that directly compares binge drinking and daily alcohol consumption for metabolic diseases.

And I suspect that we will not have a RCT on this issue. But, but that's the point about alcohol and metabolic liver disease. And to continue the NHANES study, do we know how much alcohol they actually drank? Yes, again, everything is self-reported. So it's possible that's what they were drinking. It is also possible that this is a slight understatement. I believe men drank about 40 to 60 grams a day, and women needed a little less. We'll put the exact numbers on the show notes page, but what that means is that these are people who self- report three, at least three drinks a day, maybe four drinks a day.

Um, because again , 60 grams of ethanol is technically–that's, well, for a normal-sized drink or potentially less if you're drinking, you know, if you're pouring it yourself. Sorry. I mean, I would also like to add, Nick, that there are many people who can drink that amount of alcohol and they are fully functional. So I do n't want the interpretation to be that this only applies to people, you know, who are heavy drinkers, because a lot of people can have three drinks a day and obviously not have any obvious, uh, side effects from it.

Going beyond just lifestyle, when looking at the liver, are there people who are at higher risk at the start of the study, whether it's due to genetics, hormones, or something else? Yes. I would divide them into two groups. There's an inherited genetic component, and then obviously a hormonal component , which can fluctuate over time. So, on the inherited side, the most important single gene variant here is something called PNPLA3. And people who carry two copies of a particular variant tend to have about twice the risk, uh, or likelihood of fat accumulation in the liver.

And with this comes an increased risk of inflammation and fibrosis, even after taking into account standard metabolic risk factors. Hmm, there are also variants that seem protective, particularly a loss-of-function variant in a gene called HSD17B13, which is associated with reduced liver enzyme levels and risk of fibrosis, and it may partially offset the risk associated with PNPA3. There are also other options. Again , we'll list them in the show notes for completeness, but I think the main point here is that there is an absolute genetic predisposition and even some protection that we see.

Hmm, and that, I mean, I think any clinician can confirm that, right? You have a patient where for some reason two people do the same things and they have completely different liver conditions. Hmm, that's why ancestry can manifest itself in population-level risk, although, you know, we have to be careful not to exaggerate it. Therefore, the PMPA3 risk variant is much more common in people of Hispanic descent. That's why, at a population level, we know that Latinos are much more sensitive and therefore prone to masolda and purée.

Hmm, and it's actually the opposite for people of African descent. So, that probably continues to influence what we see clinically. But again, that doesn't mean that on an individual level. It's always like this. So I don't want anyone listening to this who is black to think, great, I can't get mass, you know, I'm leaving. And I don't want any Latino listening to this to say, "Oh , well, that's great. This is my destiny." Hmm, it's just, again, it's predisposition, but it's, you know, it's not fate.

So I mean, now there are also differences in body composition that standard lab tests and BMI data can always miss. For example, many people of Asian descent develop metabolic risk at lower and normal BMIs, partly again because visceral atypia may be higher at a given body weight in a group of people who otherwise do not genetically accumulate much subcutaneous fat. So again , this is why I believe that body weight and BMI, while useful tools at the population level, offer nothing at the individual level .

I wouldn't be able to tell you the BMI of one of my patients, but I can tell you almost every one of their measurements, um, total body fat, visceral fat, and other more nuanced ones. That's what's really important. Another important baseline modifier is menopause. So premenopausal women are relatively protected. Um , the net effect of estrogen here seems to be inhibiting the accumulation of visceral and epithelial fat. Um, of course, after menopause, that protection starts to fade, and it can happen quite quickly, and then fatty liver disease becomes more prevalent and can progress, um, actually, more aggressively.

So, again, all of these things: ancestry, family history, genotype, um, the whole menopausal status, all of that goes into the risk assessment. Hmm, but again, none of these replace the main question, which is : what is the actual metabolic phenotype of a person. So I don't want to get too hung up on what increases or decreases risk, other than what I just said. I think what we really want to focus on is how do you actually objectively measure this in yourself in a unique way? Peter, let's get to this, which is how people define the health of their liver in a certain way.

So, I think if you ask most people, they would assume that if they get a blood test every year and their liver enzymes come back to normal, then their liver is fine. So, first of all, would you say this is true? Thank you for watching this episode of " Ask Me Anything" of The Drive. As a premium member, you will get immediate access to the full AMA episode. You just previewed our entire catalog of AMA episodes and all upcoming AMA episodes. You will receive premium longevity-focused articles with useful information .

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