Taking control over your eating habits is a noble cause, but like most good things, it does require some perseverance. Verywell Fit explains that after the first few days of a low-carb diet, some people encounter a set of symptoms often referred to as "low-carb crash" or "keto flu". Harvard Health Publishing asserts that the condition has neither been recognized by the medical community nor substantiated by scientific research, but the phenomenon is widely discussed on the internet in articles, blogs, and online forums.

So while we can't say for certain why keto flu happens, Verywell Fit offers up the theory that it occurs when the body has used up the last of its glucose reserves, which are stored in the liver as glycogen, but has not yet adapted to getting energy from fat and protein.

Healthline explains that while some people kick carbs without any side effects, others have reported symptoms including nausea, headache, diarrhea, dizziness, weakness, muscle cramps or soreness, difficulty sleeping, poor concentration and irritability, and sugar cravings.

Continued here:
Is Carb Withdrawal A Real Thing? - Health Digest

Mindy Kaling is showcasing her incredible weight loss journey in a gorgeous blue swimsuit, saying she is excited to show off her new look. "The lowkey romantic gift my friends @traceywigfield and @loulielang gave me was this sexy blue one piece bathing suit which I was so excited to model. You know you have good friends when they're excited to buy you intimate apparel!," she captioned an Instagram post. How does she stay so fit? Read on to see 7 ways Kaling stays in shape and the photos that prove they workand to get beach-ready yourself, don't miss these essential 30 Best-Ever Celebrity Bathing Suit Photos!

Kaling is passionate about not being too restrictive with diet, as it usually backfires. "I eat what I like to eat," the actress told ET. "If I do any kind of restrictive diet, it never really works for me. I just eat less of it." Experts agree that severely restrictive diets rarely work over the long term. "At any given time, more than a third of Americans are on a specific diet, with weight loss as a leading reason," says Robert H. Shmerling, MD. "Most are going to be disappointed, because even when successful, lost weight is frequently regained within a few months."df44d9eab23ea271ddde7545ae2c09ec

While Kaling refuses to diet, she understands moderation is crucial for health. "I'm never going stop being a foodie. I'm never going be someone who can just have spinach and salmon every day," Kaling says. "I just am really for the first time in my life, trying moderation, and I love it."

Kaling makes a point to keep moving throughout the day. "Sometimes I'll be like, 'Well, I have four different times today where I have 10 minutes so let's just walk instead of sitting down and checking Instagram,'" she says. "So instead of it being like one chunk of exercise in the beginning of the day or none at all, I'm now just deciding that I'm going to be a more active person all the time."

Kaling understands that when it comes to exercise, it's important to find something you enjoy."In my 20s, I thought a workout had to be something that was punishing, like 45 minutes of running and you had to hate it the whole time," she says. "I don't have that relationship with exercise anymore."

Like most people who instinctively understand what works for their body, Kaling doesn't overthink her diet and fitness regimen. "Honestly, I didn't really do anything differently. I eat what I like to eat. If I do any kind of restrictive diet, it never really works for me. I just eat less of it I wish there was something more juicy or dynamic about the way that I've lost a little bit of weight, but that's the way I've done it," she explains.

Kaling appreciates the mental health benefits of exercise. "I love working out," she says. "I don't go to therapy, and I think that's because I get endorphins from exercise. It's such a powerful tool for me mentally. I know that working out is not the path for me to be skinny. For my body type, that entails eating well and making healthy choices. Working out is a way for me to have mental strength, and now, with a kid, it's also time that I have just for myself and to focus on my body."

Kaling continued working out throughout her pregnancy to make post-baby weight loss easier. "I did a lot of yoga and a lot of walking, and I jogged until I couldn't jog anymore," Kaling says. "I exercised until the morning I gave birth. Also, about a week after I had the baby, I started walking a couple of miles a day. I don't recommend that for everyone, obviously, but I didn't have that difficult of a delivery. All those things were really helpful when it came to losing the weight."

Link:
Mindy Kaling in Bathing Suit is "Excited to Model" Celebwell - Celebwell

Shifting guidelines, lack of access to insurance, and a failure to focus on lifestyle as the primary tool to manage hypertension have allowed the United States to lose ground in the battle for blood pressure control, according to 3 of the countrys leading experts on cardiovascular and kidney disease who spoke during the recent 2022 Congress of the American Society for Preventive Cardiology (ASPC), held July 29-31 in Louisville, Kentucky.

Keith C. Ferdinand, MD, professor of medicine at Tulane University School of Medicine; Kim Allan Williams, MD, who last month became the chair of the Department of Medicine at the University of Louisville; and George C. Bakris, MD, professor of Medicine and director, Comprehensive Hypertension Center, University of Chicago Medicine, spoke about different aspects of hypertension treatment and access to careand how management of hypertension is essential to avoid chronic kidney disease (CKD).

Bakris said that in 2014, improvements in treatment had allowed blood pressure (BP) control rates among US adults to reach 53.8%, up from 31.8% in the early 2000s. Williams explained how the Joint National Committee 8 guidelines (JNC 8) in 2014 included a hotly debated recommendation to not initiate treatment for hypertension for patients over age 60 until BP reached 150/90; this contributed to a nosedive in control rates, until they hit 43.7% in 2018.

Then in 2015, the SPRINT trial, funded by the National Institutes of Health, showed beyond a doubt that controlling BP to below 140/90, even down to 121/80 dramatically reduced heart attacks, strokes, and cardiac deaths with limited effect on acute kidney injury, from which patients recovered. Williams retraced how the findings propelled the American College of Cardiology (ACC) and the American Heart Association (AHA) to execute new BP guidelines in 2017 that list BP just above that level as elevated and BP that reaches 130/90 as Stage 1 hypertension.

Confusion over guidelines played a role in the United States regression in BP control, but Bakris said that doesnt tell the whole story. He noted in sharing a global report card on hypertension that the countries with the best rankingsCanada, Costa Rica, South Korea, and Taiwanall had universal health coverage. Thats not a political statement. Thats just a fact, he said.

Ferdinand, who spoke a day prior to Williams and Bakris during a symposium on womens heart health, also raised the issue of access to insurance coverage for at-home BP monitors. Williams and Ferdinand agreed that hypertension cannot be properly diagnosed and managed without out-of-office BP readings. Besides the well-known white coat effect, which can lead to higher-than-normal readings in the physicians office, the phenomenon of masked hypertension can cause some patients to have lower readings when away from stressful home environment.

Ferdinand discussed findings from a small, unpublished sample that showed when patients had access to a BP device and at-home results were transmitted to the clinic via Bluetooth technology, Were able to show increased adherence and improvement in blood pressure.

Hypertension and Disparities

Ferdinand reviewed why hypertension is so important in addressing health disparities: although longevity has increased overall prior to the pandemic, the shortest life expectancy among the major racial/ethnic groups are the non-Hispanic Black populations.

The White-Black gap has been present for decades, he continued, and COVID-19 has only made the gap worse. And the protective effect of being Latino has been lost.

Meanwhile, Hypertension in the Black population is perhaps the most powerful risk factor, he said, tracing data that show how it appears first among males but then rises over time among females, until the disease burden is significantly higher among women as they get past age 60. Loss of estrogen between age 50 and 60 is a factor for increased hypertension in older women, Ferdinand said.

Williams continued this theme. If we can just control hypertension, were going to do so much better, he said. We know what it does, and if we focus on the fact that our ethnic disparities really weave their way through hypertension, starting with renal disease and congestive heart failure, the need to keep BP levels below 140/90 to reduce the risk of cardiovascular mortality makes sense.

Hypertension is the most powerful and potent predictor for morbidity and mortality both in men and women, but even more so in womenespecially in older women, Ferdinand said. Combination drug therapy is now the best practice in order to control blood pressure, and we need more attention to hypertension and appropriate diversity in research.

Starting With Lifestyle

Williams, who has long advocated plant-based diets, addressed criticism that the 2017 ACC/AHA update to the blood pressure guidelines was a way to get patients to take more medication. We werent recommending more drugs for a lot of people, he said. We were talking about lifestyle.

Williams spent most of his talk on the need to give more attention lifestyle change, including weight loss, smoking cessation, and limiting alcohol consumption. But I always like to focus on dietary evidence, he said.

Theres abundant evidence in support of the DASH diet (Dietary Approaches to Stop Hypertension), but not everyone looks at the DASH diet the way I do. he said.

The key takeaways from the many studies are that diets with less fat and less cholesterol, which are more towards a vegetarian, non-exclusive vegetarian dietthat gives you the largest impact on blood pressure.

More studies have accumulated about the mechanisms of why these diets work as an intervention. Some of them are very strong, some of them are less strong, but the data is really bending toward the more intervention you do with plants, the better off you're going to be. And I'm irritated that we've had to say it for quite a while, we just didn't know exactly why.

However, in the last 3 to 5 years, thats changed. Its all about the microbiome, Williams said, offering a primer on microbiologyand how the bacteria, fungi, and viruses, which help digest food and make up a persons immune system, are affected by the environmentin other words, by the people around them. This was seen during COVID-19, he said, as people who ate a lot of red meat got very sick.

When it comes to hypertension, he said, a major factor is, What species do you have in your microbiome?

Bakris, who followed Williams, agreed. One factor that makes kidney disease such a major cardiovascular risk factor, he said, is that when the estimated glomerular filtration rate (eGFR) gets down to the 40s (90 is normal; below 15 is kidney failure), the microbiome totally changes and becomes very cardiotoxic.

Flurry of Activity in Drug Pipeline

Medication adherence is a known problem in managing hypertension, but so is measuring BP correctly, which gets less notice. We are not paying attention to very simple things, Bakris said.

Hypertension has been perceived as dead for the last decade, because nothing really new is happening, he said. But theres a huge flurry of activity coming in the next 5 to 7 years specifically in resistant hypertension.

He highlighted the current recommendation for resistant hypertension, published in 2018 for the AHA, which calls for:

However, he noted that these recommendations were based on a trial where patients had close to normal eGFR; most patients with advanced hypertension also have advanced CKD, with eGFR in the 40s. Its not so easy to go to spironolactone(an MRA) with potassium issues, he said.

Its important to keep in mind what could be coming soon. He discussed:

Nonsteroidal MRAs. Bakris said these agents have a very different chemistry from MRAs with far less adverse effects. He mentioned finerenone, already approved as Kerendia to reduce renal and cardiovascular risks in patients with type 2 diabetes. The gossip is it doesnt lower blood pressure, he said, Well, it actually does, and the papers are in press.

He focused discussed several possible therapies being studied for resistant BP, including ocedurenone, which he said, lowers blood pressure significantly and has a very good pharmacological profile.

Bakris then discussed the BLOCK-CKD trial involving KBP-5074, an investigational agent being developed by KBP Biosciences. Results of the phase 2b study in patients with stage 3b/4 CKD showed a reduction of 10.2 mm Hg compared with placebo of systolic BP at the larger dose (0.5 mg), with some elevation of hyperkalemia.

Like other speakers at ASPC, Bakris warned that albumin, not just eGFR, must be monitored to catch CKD at early stages.

Endothelin receptor agonists. Therapies in this class are already approved to treat pulmonary arterial hypertension (PAH), but Bakris said whats coming is a joint endothelin A/endothelin B receptor agonist. He urged the audience to look forward to results from the PRECISON trial, studying aprocitentan.

Brain aminopeptidase inhibitor. Bakris said the first drug in this class, firibastat, appears to offer more benefit in treating hypertension to Black patients, although the reasons for this are unclear.

Angiotensinogen knockouts.Yet another approach is to target angiotensinogen, which would address hypertension by addressing overactivity at the top of the reninangiotensin-aldosterone system pathway. According to an article in JACC: Basic to Translational Science that Bakris cited, the idea is to go after the RAAS pathway at its source, rather than downstream which is how angiotensin-converting enzyme inhibitors or type I angiotensin receptor blockers work.

So, weve left the kidney; weve left the vessels, and weve moved into the liver, Bikras said.

He cited an article that presented phase 2 results for IONIS-AGT-LRx, which is being developed for hypertension and heart failure indications. Early data for a therapy that would treat BP by injection for up to 6 months are promising very promising, but Bakris noted the need for reversal agent, which he said is being addressed.

In the near term, Bakris expects the FDA to consider renal denervation, a process that removes nerves from the renal artery. This is already approved in some parts of Europe.

With at least 4 different classes of BP lowering agents in the pipeline, he said, I'm confident that over the next 3 to 4 years, there's going to be a lot more in the armamentarium to use, to get the blood pressure lower with fewer side effects than what we have right now.

Read more:
As Health Disparities Weave Their Way Through Hypertension, New Agents Are on the Way - AJMC.com Managed Markets Network

By Simon Spichak, MSc | August 4th, 2022

As we age, cognitive function declines. In some people, this process happens faster than others. Mounting research points to the idea that highly processed foods with lots of calories, salt, fat and added sugars think: sugary sodas, grocery store birthday cake, fast food burgers and fries may cause older adults cognitive abilities to decline faster.

At the Alzheimers Association International Conference this week, Natalia Gonalves, PhD, from the University of So Paulo Medical School presented research that compared the cognitive health of older adults who frequently partook in foods that contain few to no unprocessed ingredients against the cognitive health of those who ate more than 80 percent healthy foods.

The main takeaway is that diet is a modifiable lifestyle factor, Gonalves told Being Patient. Therefore, we can choose to make better dietary choices in order to protect our brain health long term.

The study tracked 10,775 people with an average age of 50 in Brazil for up to a decade, finding that people who ate lots of ultra-processed food their diets were made up of 20 percent junk food at the start of the study were more likely to experience declining decision making abilities and declining ability to learn, remember and focus on things overall as they aged. The research has now been submitted to scientific journals for peer review.

The findings support past evidence that highly processed junk food i.e. higher cholesterol, more sugars is associated with worse cognitive health. This preliminary work builds on other larger studies that have found older adults who ate more unhealthy foods had a smaller hippocampus, the region of the brain responsible for memory, which may lead to more memory difficulties or other cognitive challenges.

On the flip side, however, mounting evidence supports the idea that health diets like the MIND or Mediterranean-style diet, which are low in processed foods, and high in vegetables, olive oil and omega 3s improve brain health. Studies repeatedly imply that something about these diets helps to protect the brain from cognitive decline and Alzheimers.

In both cases, the science isnt there yet to call these associations proven. Diet studies are often clouded with parallel lifestyle variables that are tough to control for. But Alzheimers Association Senior Director of Scientific Programs and Outreach Claire Sexton said while research continues, people have little to lose in taking up a healthier diet.

There is growing evidence that what we eat can impact our brains as we age, and many studies suggest it is best to eat a heart-healthy diet low in processed foods, and high in whole, nutritional foods like vegetables and fruits, Sexton said in a news release.

Future work is on the way to help clear up the complicated links between food and memory, uncovering why we might really be what we eat.

Visit link:
Processed Foods (Like Ice Cream) Hurts Brain Function, Study Finds - Being Patient

ITS come home all thanks to the Lionesses.

And now fans have a new season and the World Cup this winter to look forward to.

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Theres no doubt the physical demands of the beautiful game are gruelling for players in the top flight.

But what might surprise you is that you too can follow their lead when it comes to healthy eating.

Performance nutritionist Liam Holmes has worked in elite sport for 12 years, and has helped footballers at Tottenham Hotspur, Fulham and the Republic of Ireland national team.

Liam, who is currently working with Celtic and owns pH Nutrition, tells Sun Health: To achieve the fitness levels and get in the shape that pro footballers are in, it comes down to one thing consistently eating the right things.

Here, Liam breaks down what a professional footballer eats and reveals nutrition tips for you to focus on.

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CARB loading isnt a myth its still something players do. Its just a lot more controlled than back in the eat all the pasta possible days, Liam says.

I encourage the players I work with to make this meal fairly similar each time you dont want to be experimenting the night before the match, he adds.

Most players will eat the exact same meal the night before a match every single time.

If you are planning a big workout or have a big football match, I always advise this strategy.

Their meal will consist of a large serving of carbs such as rice, potatoes, grains or breads, accompanied by a portion of lean protein and vegetables.

This balanced meal helps top up energy stores ready for the match whilst providing micronutrients for recovery.

THE main focus for match day is topping up, Liam explains.

Players are advised not to overload their bodies by trying to eat lots of calories ahead of a match, he says. We dont want players to still be digesting their meal in the warm-up.

What players eat will depend on the time of the match, but a typical pre-match meal will tend to consist of a small serving of lean protein, some simple carbs like a handful of brown rice, a few veggies and a small serving of fat, like cheese or avocado.

Players are encouraged to eat low-fibre carbs such as rice, pasta and bread with easily digestible veg like peas, corn and carrots so they feel light and ready to go by the warm-up.

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THERES a good reason the player of the match doesnt get champagne anymore, Liam explains.

Alcohol is not a good idea immediately after a game, he says.

Its important that players follow the three Rs rehydrate, repair and replenish.

Players will take some form of recovery shake, which includes protein, electrolytes and carbohydrates to kick-start the process.

Lots of protein shakes now include all of these as standard so you can easily have these yourself.

We then advise players to eat a meal 60 to 90 minutes after a match with protein, carbohydrates and vegetables. Usually appetite is suppressed after a game so using finger food-style meals or smaller dishes can help get players to eat.

TO ease muscle pains and boost energy levels, players usually start the day with eggs, Greek yoghurt, nuts, berries, smoothies and beans, Liam reveals.

And after a morning of stretching and massage, lunch continues the recovery theme.

Salmon, beef, chicken thigh, potatoes, grains and lots of fruit and veg are on the menu, he says.

It is key on these days to make sure protein intake is consistent across the day, to aid muscle repair, so players will snack once or twice in the afternoon before dinner and then before bed.

The pre bed snack will usually be Greek yoghurt and fruit or cottage cheese and oat cakes to provide slow releasing protein overnight and aid recovery even further.

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THIS might come as a surprise but nothing is really off-limits for pro footballers.

Liam says: Alcohol is usually removed as much as possible and if the players do have a drink then they usually wait until off season.

Players need variety in their diets to get ultimate nutrition, so away from matches they can add in their favourite foods.

That said, they are advised to avoid and most do deep-fried food, very oily food like chips, sweets and processed foods like biscuits, crisps and cakes.

They avoid these ultra-processed foods because they have little to no nutritional qualities and they can contribute to inflammation something that we actively want to avoid as much as possible for footballers, Liam adds.

TOP players are human, and like the rest of us they need to snack.

Trying to sneak anti-inflammatory foods in is something we try to encourage players to do when they are snacking, says Liam.

Dark-coloured fruits such as berries, green veg, oily fish such as salmon, tomatoes, peppers and spices can all help recovery.

HOLIDAYS are a time to treat yourself even if youre a top-flight player.

These days its true that players are far more conscious of the effects of alcohol and poor-quality food even while on holiday, Liam says.

But in the off season players naturally are more relaxed when it comes to the foods they limit during the season.

They will make sure they eat a balanced diet still, but might sneak in a few biscuits and crisps.

Due to the demands of elite football now there is less time off so the players still need to be eating well to support recovery.

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GOOD news if you want to emulate the top flight, theres no need to ditch your morning cuppa.

Caffeine is one of the most researched performance-enhancing substances available for players to use, Liam says.

It can help endurance, sprint performance and decision-making so most players drink coffee but time when they drink it specifically around training and matches.

Taking caffeine in a coffee or energy drink 45 to 60 minutes pre-match or pre-training can help performance.

Footballers also really prioritise their sleep so they are wary of drinking coffee past 2pm because it can interrupt your ability to sleep.

YOU might be surprised to hear cake is a very necessary part of a players diet.

Being on the ball with your nutrition seven days a week for an entire season is impossible, even for the best players.

And while chowing down on a few doughnuts just before a match is not advised, Liam explains the high-sugar treats have their place.

He says: Things like cakes and sweets are very energy-dense, so it can actually help when replenishing energy stores during tough periods of matches as they are usually high in carbohydrates.

So it isnt completely unheard of anymore for players to enjoy a cake, biscuit or even cheesecake as it is also high in protein at half time.

The rest is here:
Im a nutritionist heres what I tell all Premier League footballers about their diet and how you can cop... - The US Sun

KEY POINTS

.. there are things we know we know. We also know there are known unknowns; that is to say, we know there are some things we do not know.

Donald Rumsfeld

In 1973, Dr Robert Atkins was called to testify before the US Senate Select Committee on Nutrition and Human Needs [1]. The committee was charged with investigating, amongst others, the eponymously named high fat Atkins diet, which was considered nutritionally unsound and potentially dangerous. Nutrition experts called upon were unanimous in their testimony that this diet was potentially harmful. Dr Fred Stare, for example, Chairman of Harvard's Department of Nutrition stated any diet which tends to be high in saturated fat and cholesterol tends to elevate the chance that the individual will get heart disease. (pg 17). This viewpoint on the potential hazards of the Atkins diet was expressed that year in an editorial in JAMA which stated, Perhaps the greatest danger (of the Atkins diet) is related to hyperlipidemia, which may be induced by such a regimen which could be responsible for accelerating atherosclerosis [2]. These concerns with an Atkins, that is, low carbohydrate diet (LCD) expressed 50 years ago have persisted, as evidenced by the recent proclamation by the National Lipid Association Nutrition and Lifestyle Task Force, that long-term consumption of the LCD increases the risk of all-cause and cardiovascular mortality [3].

Concerns with the safety of the LCD are based, in part, on the diet-heart hypothesis, which postulates that unrestricted consumption of saturated fat (from animal fat and tropical oils) on an LCD may raise serum cholesterol levels, thereby increasing one's risk of developing cardiovascular disease (CVD) [46]. This hypothesis, however, has failed to receive empirical support, with decades of scholarly critiques of its flaws [717,18,1921]. We concur with DuBroff and de Lorgeril [7] that the diet-heart hypothesis survives only because its proponents selectively cite evidence that validates their own viewpoint while disregarding evidence to the contrary.

An extension of the diet-heart hypothesis is the view that an elevated level of low-density lipoprotein cholesterol (LDL-C), under any circumstance, is unequivocally recognized as the principal driving force in the development of (atherosclerotic cardiovascular disease) [22] and that the key initiating event in atherogenesis is the retention of low-density lipoprotein (LDL) cholesterol (LDL-C) within the arterial wall [23]. This perspective on LDL-C as inherently atherogenic has been the driving force in recent concerns that an LCD-induced increase in LDL-C increases one's risk for developing CVD [24,2528,29,30].

Regarding an increase in LDL-C on an LCD in relation to the risk of a coronary event, we shall paraphrase the quote from Donald Rumsfeld by stating there are known knowns and known unknowns about LCD, LDL-C, and CVD. It is known that the LCD improves many CVD-relevant biomarkers, but it is not known with certainty if an increase in LDL-C on an LCD is proatherogenic, neutral or beneficial. The basis of our lack of knowledge on this issue is the absence of any published long-term clinical trials which have characterized hard coronary events, for example, myocardial infarction, stroke or coronary death, in people who develop high LDL-C on an LCD. Therefore, despite the concerns expressed repeatedly over the past 5 decades, there is no conclusive research to indicate whether an increase in LDL-C for someone on an LCD has any effect, beneficial or harmful, on CVD outcomes.

We have approached the issue of LDL-C concerns on an LCD with the following strategy. First, we have evaluated the dogmatic view held by various heart disease organizations that high LDL-C is inherently atherogenic [22,23,31]. Second, we have reviewed research on measures which are superior to LDL-C, such as insulin resistance (IR) and LDL particle subtypes, as markers of CVD risk. Third, we have reviewed findings that demonstrate the LCD improves all biomarkers which are strongly associated with CVD. Lastly, while there is active debate about the merits of statin therapy in primary prevention of CVD [3234], statin therapy in secondary prevention trials and in high risk populations, such as those with type 2 diabetes, have reported a small coronary event and mortality absolute risk benefit [3537,38]. We have addressed whether this modest benefit of statin treatment can be attributed to the lowering of LDL-C, per se, or through other mechanisms. More importantly, we have evaluated whether the benefit of statin treatment reported in clinical trials can be extended to people on an LCD with elevated LDL-C.

In 1985, Brown and Goldstein received the Nobel Prize for their research on LDL-C in people with familial hypercholesterolemia (FH). They discovered that this genetic condition involves impaired binding of LDL to its membrane receptor, which results in dramatically elevated serum levels of LDL-C. Because people with FH exhibited premature CVD, Brown and Goldstein declared there was a causal relation between an elevated level of circulating LDL and atherosclerosis [39], thereby providing support for the lipid hypothesis, in which LDL-C is described as inherently atherogenic. Since then, this pejorative view of LDL-C as the bad cholesterol has been promoted by high profile heart disease organizations, such as the American Heart Association [40], as well as the European Atherosclerosis Society, which states LDL is unequivocally recognized as the principal driving force in the development of ASCVD (atherosclerotic cardiovascular disease) [22].

Studies on the FH population, however, provide an extensive literature highlighting inconsistencies with the lipid hypothesis. For example, if LDL-C is inherently atherogenic, the burden of atherosclerosis should increase with the time of exposure to LDL-C. That is, cardiovascular mortality would be predicted to increase with age as a direct consequence of the time of exposure to LDL-C. To the contrary, CVD mortality in FH individuals declines with age [41]. Elderly individuals with FH exhibit an equivalent risk of CVD mortality to those in the non-FH population, despite a lifetime of exposure to high LDL-C. This finding directly conflicts with the dual component hypothesis that LDL-C is inherently atherogenic, and that CVD risk increases with the duration of LDL-C exposure [42]. That elderly FH individuals exposed to decades of high LDL-C demonstrate no increase in CVD mortality, as well as no increase in morbidity, for example, ischemic stroke [43], compared to the general population, undermines the lipid hypothesis, that is, that high LDL-C is inherently atherogenic.

Further challenging to the lipid hypothesis is that FH individuals have a lifetime all-cause mortality rate which is equivalent to, or even lower, than that of the general population [41,4447]. We submit three explanations for the longevity of people with FH. First, the small subset of individuals with FH that die prematurely of CVD appear to be genetically susceptible to develop coagulopathy, independent of their LDL-C levels [48,4951]. In one example, Jansen et al., [51] reported that whereas LDL-C did not differ between CVD and non-CVD FH patients, those with a polymorphism for the prothrombin (coagulation factor II) gene exhibited over twice the incidence of CVD than those without the polymorphism. Second, LDL-C is an important component of the immune system [5254]. Chronically elevated LDL-C levels may enhance aspects of immune functioning, thereby lowering rates of mortality from cancer and infection [41,46,47]. In related work, elevated LDL-C may protect against bacterial infection, which can promote the development of atherosclerosis [53,5560]. Third, FH individuals, either through lifestyle choices or favorable genetics, have a relatively low rate of type 2 diabetes [6165], which itself is a significant risk factor for CVD. These three observations help to explain why FH individuals do not face an increased risk of CVD mortality with advanced age, as well as the greater longevity of people in the general population with high LDL-C, compared to those with low LDL-C [66].

Despite several influential heart disease organizations holding the position that LDL-C is a cause of CVD, it has long been recognized that LDL-C is a poor marker of risk for CVD [6769,70,71], as well as cardiovascular and all-cause mortality [66]. For example, calcification within the coronary arteries, in contrast to LDL-C, is a reliable measure of CVD risk. Coronary artery calcium (CAC) scoring has proven to be the single best predictor of fatal and nonfatal coronary events [7275], including CVD risk in diabetic and nondiabetic patients [7678], as well as in young, mid-age and elderly patients [79]. CAC scoring also excels at long-term risk prediction over periods of more than a decade [76,78,80]. Moreover, among those with genetically confirmed FH, approximately half showed no detectable CAC and had a favorable prognosis, despite significantly elevated LDL-C levels [81].

The superiority of CAC to LDL-C in relation to plaque development, as well as coronary events, in high-risk patients was demonstrated recently by Mortensen et al.[82]. These investigators identified CAC levels as being superior to, and independent of, LDL-C, as a biomarker of coronary event rate. In related work, Miname et al.[81] reported that coronary events in statin-treated patients were associated with increased CAC scores, and were unrelated to on-treatment LDL-C. Moreover, these investigators found that the ascending gradient of CAC scores was associated with increases in fasting glucose and not in on-treatment LDL-C values.

In one representative example of the value of CAC scoring, Sandesara et al.[83] reported that over one third of individuals with very high LDL-C (>190 mg/dl) had a zero CAC score. Hence, the zero CAC score had more predictive utility than LDL-C because these individuals had a very low risk for future coronary events. These findings, as well as related research, were discussed by Bittencourt et al.[84], who concluded treatment of individuals with very high LDL-C (>190 mg/dl) irrespective of their clinical risk might not be the most prudent approach . These investigators further noted that low CAC scores, and therefore the low CVD risk, in individuals with very high LDL-C should make us question at least part of our understanding of the atherosclerotic process.

In addition to CAC scoring, serological markers have demonstrated clear superiority to LDL-C levels in assessing CVD risk. For example, Yu et al.[85] reported that markers of the insulin-resistant phenotype, specifically elevated fasting plasma glucose, hemoglobin A1c and triglycerides (TG), were all positively correlated with the severity of coronary stenosis; LDL-C levels, in contrast, showed no correlation with coronary stenosis. In another example, FH individuals that carry an A, B or AB blood group (which is associated with increased coagulation [86]), have a twofold increased risk of CVD, compared to those with blood type O [87].

Often overlooked in the discussion about LDL-C as a cardiovascular risk factor is the heterogeneity of different LDL particles. That is, the total LDL-C reported in a conventional lipid panel represents the sum of a heterogeneous population of different low-density lipoprotein particles [71]. One unique population of LDL particles is known as lipoprotein (a) (Lp(a)). Lp(a) is a modified LDL particle in which an apolipoprotein (a) molecule is covalently attached to the ApoB100 moiety of an LDL particle. The link of Lp(a) to CVD may be driven by its pro-inflammatory effects [88]. Lipid peroxidation colocalizes with Lp(a) to contribute to the pathogenesis of CVD by promoting endothelial dysfunction, lipid deposition, inflammation, and arterial calcification [89]. This research has provided strong support for the view that an elevated plasma concentration of Lp(a) is an independent risk factor for the development of CVD in FH and non-FH individuals [9094]. It is notable that Willeit et al.[95] recently reported that correcting for the Lp(a) component in the total LDL-C measure eliminated isolated LDL-C as a CVD risk factor. This refined assessment of LDL-C, which takes into account the Lp(a) subfraction, provides a mechanistic basis for why LDL-C is a poor marker of CVD risk.

In summary, the pejorative view of LDL-C as the bad cholesterol, which is inherently atherogenic, is not supported by a balanced review of the literature. Numerous investigators who have assessed the clinical literature have concluded that the lipid hypothesis persists today only because of the biases of its proponents [49,67,68,96,97]. Characteristic of this sentiment is the opinion that evidence falsifying the hypothesis that LDL drives atherosclerosis has been largely ignored [98], and the perspective of three cardiologists that LDL cholesterol risk has been exaggerated - Decades of emphasis on the primacy of lowering plasma cholesterol, as if this was an end in itself, has been misguided. [21]. Finally, the negative impact of the emphasis on LDL-C reduction in developing therapeutics has also been recognized, leading DuBroff [96] to conclude that the LDL-C-centric approach to cardiovascular disease prevention may have distracted us from investigating other pathophysiologic mechanisms and treatments.

There is an extensive literature demonstrating that biomarkers other than LDL-C provide more reliable assessments of CVD risk. Furthermore, mechanisms have been clearly described for these biomarkers, affording biological plausibility. Of these other risk factors, IR, which is related to hyperinsulinemia and hyperglycemia, is perhaps the most important. Over 3 decades ago, Gerald Reaven summarized the research on IR by stating that the physiological attempt to compensate for IR sets in motion a series of events that play an important role in the development of both hypertension and coronary artery disease, and that variations in insulin-stimulated glucose uptake determine to an enormous degree the likelihood that an individual will develop premature atherosclerotic vascular disease [99]. Kraft's [100], conviction that those with CVD not known to have diabetes were simply undiagnosed revealed his insight into the core mechanisms of CVD. Contemporary research has confirmed that IR is a strong and independent predictor of CVD, with compelling evidence that IR is a major causal influence on the pathophysiology of CVD [101105]. This is driven in no small part by the causal role of IR in the development of type 2 diabetes, itself being the greatest risk for CVD [106].

There are myriad mechanisms whereby IR contributes to the pathogenesis of atherosclerosis. IR-related measures that are well established independent risk factors for CVD include hypertension [107], glycocalyx disruption secondary to hyperglycemia [108], prothrombosis [109], advanced glycation end product associated endothelial dysfunction [110] and impaired nitric oxide synthesis [111]. These IR-related mechanisms contribute to adverse effects on blood vessel structure and function [102,103,112].

Through multiple distinct mechanisms, IR is often the primary driver for hypertension [113,114], including stimulation of sodium retaining channels within the nephron [115], as well as activation of the sympathetic nervous system [116118]. The chronic hyperinsulinemia that occurs concurrently in IR promotes chronically elevated epinephrine, which elicits cardiovascular activation, including increased cardiac output and systemic vasoconstriction [119,120], as well as an enhancement of platelet aggregation [121].

IR-associated hyperinsulinemia is also associated with CVD risk through increased macrophage lipid accrual in blood vessels. As macrophages accrue lipids, they become foam cells. Foam cells are a staple feature of atherosclerotic plaques, not only constituting a major portion of the plaque itself, but also contributing to atherosclerosis by aggressively secreting pro-inflammatory cytokines [122]. Park et al.[123] demonstrated that insulin increased macrophage oxidized LDL uptake by more than 80% and produced almost three times greater total lipid uptake into the macrophage in as little as 16 h.

IR, and more specifically, type 2 diabetes and obesity, are associated with serum lipid components which are well established risk factors for CVD. Specifically, LDL-C is contained in heterogeneous particles which range in size and composition from a small dense LDL (sdLDL) to a large buoyant LDL (lbLDL) (which is distinct from the inclusion of Lp(a) in the total LDL-C measure, as discussed previously). Circulating sdLDL, unlike lbLDL, readily undergoes atherogenic modifications in plasma, including glycation, which is associated with heightened inflammation, hyperglycemia, and an increased incidence of CVD in the general population [127130], and in FH individuals [131,132].

The distinction between LDL particle subclasses based on size and density is also important because sdLDL is a component of the atherogenic dyslipidemia risk triad, composed of elevated levels of TGs and sdLDL, in concert with low HDL-C [124126]. High TGs, elevated sdLDL and low HDL-C are each, individually, strong markers of CVD risk [71,89,133142]. Conversely, lbLDL has not been shown to be a CVD risk factor, as demonstrated in the Atherosclerosis Risk in Communities Study [143], the Quebec Cardiovascular Study [144], the Multiethnic Study of Atherosclerosis [145] and the Framingham Offspring Study [146]. Ultimately, the assessment of sdLDL and lbLDL subpopulations provides a greater prediction of CVD risk than does LDL-C [142].

The superiority of the atherogenic dyslipidemia risk triad over total LDL-C as a reliable means of assessing CVD risk has been known for more than 3 decades [147]. In 1988, Austin et al.[148] reported that individuals with the atherogenic dyslipidemia risk triad, referred to as pattern B, exhibited a threefold increased risk of myocardial infarction, independent of age, sex, and relative weight.. Even then, it was understood that total cholesterol and LDL-C were of limited value as markers of CVD risk (Fig. 1). Comparable findings were demonstrated in the Framingham Offspring Study [149], in which low HDL-C levels and elevated TGs were correlated with reduced lbLDL, increased sdLDL, and an increased incidence of coronary artery disease. Similarly, Jeppesen et al.[150] reported a significantly greater incidence of ischemic heart disease in men with the combination of high TGs/low HDL, compared to men with low TGs/high HDL, independent of whether the men had low or high LDL-C. Related work has shown that an elevated TG to HDL-C ratio is predictive of both a pattern B LDL-C profile, dominated by sdLDL, and an overall increase in cardiovascular risk [151]. Similar findings were reported by Caselli et al.[152], who reported that high TG and low HDL-C levels were associated with CVD progression, which was independent of LDL-C levels and lipid lowering treatments. In summary, the atherogenic dyslipidemia risk triad is far superior to total LDL-C as a measure of CVD risk.

In recent years, investigators have focused on LDL particle number (ApoB), rather than LDL-C, as a superior measure of CVD risk [69,153,154]. This measure, however, has significant limitations. First, it is not limited to the LDL population, with LDL particles also found on Lp(a), an independent CVD risk factor, as well as VLDL-C and IDL-C, both of which are associated with TG, another CVD risk factor [142,155]. Second, the preferential use of particle number, rather than LDL-C, does not distinguish between particle types (sdLDL, lbLDL, Lp(a)), which have been shown to be differentially associated with CVD (as described above).

The appearance of a discordance between LDL-C and total particle number, where the particle count is higher than expected, has been suggested to serve as a superior measure of CVD risk than is LDL-C [69,156]. However, the discordance correlates closely with measures of IR, for example, metabolic syndrome and diabetes [156]. In three representative trials, Otvos et al.[157], Pencina et al.[158] and Cromwell et al.[69] reported that the discordance between LDL-C and LDL particle number was superior to LDL-C, alone, as a CVD risk factor. However, patients presenting with the ApoB discordance had higher BMI, fasting glucose, and TGs, an increased incidence of diabetes and hypertension, as well as lower HDL-C, than those that were concordant. Hence, the discordance between particle number and LDL-C is merely a surrogate marker for atherogenic dyslipidemia (dominance of elevated TGs, low HDL, and smaller LDL particles) and IR (see also [159] for related review and discussion).

Atherogenic dyslipidemia is prevalent in individuals with metabolic syndrome, prediabetes, and type 2 diabetes, which is currently afflicting millions of people in the US [160]. Chronic exposure to high levels of glucose and insulin are driving factors in the development of CVD [161,162]. Modest dietary changes can be more effective in the treatment of metabolic syndrome than commonly used antidiabetic drugs in improving CVD risk [163]. Specifically, improvement in the cluster of components of metabolic syndrome is intimately connected with carbohydrate restriction in adults [164167,168,169,170,171,172,173177,178,179180,181] and in adolescents [182]. LCDs have been shown to improve other CVD risk factors, as well, such as visceral fat, blood pressure, Lp(a) and inflammation [183189]. It is therefore highly relevant that LCDs have been studied in numerous RCTs and case reports which show improvement in glucose, lipid and insulin-based CVD risk factors, including an LCD-mediated reduction in the need for hypoglycemic medication [178,190,191,192,193,194,195,196,197,198,199].

LCDs are also effective at attenuating the atherogenic dyslipidemia risk triad (reducing TGs, sdLDL, increasing lbLDL) [159,169,172,200,201]. In a randomized, parallel trial comparing the effects of an LCD to a low-fat diet (LFD) in obese adults, the LCD resulted in greater weight loss, increased HDL-C, decreased TGs and C-reactive protein than the LFD [202]. A meta-analysis concluded that compared to LFDs, LCDs significantly lowered predicted risk of atherosclerotic cardiovascular disease [203], including reductions in plasma TGs and increased HDL-C [204,205], which collectively carry a robust predictive value that dramatically outperforms LDL-C [206].

While many studies of LCDs have been relatively short-term (<6 months), there are longer-term trials and individual case reports that demonstrate the effectiveness, and sustainability of these diets [166,168,169,207209]. For example, after 1 year, a group of participants with type 2 diabetes following a ketogenic diet demonstrated robust improvements in several cardiovascular risk markers, including decreased TGs, sdLDL particles, blood pressure, and antihypertensive medications [210,211]. These findings have been replicated and extended to 23 year-long LCD trials, documenting improvements in numerous CVD risk biomarkers [212214], including a 2 year LCD intervention which demonstrated improvements in LDL particle size and carotid intima media thickness, a commonly used marker of atherosclerosis [200]. The longest assessment of LCD effects on record is by Heussinger et al.[215], who documented the safety and effectiveness of the ketogenic diet over a 10-year period in the treatment of patients with epilepsy, without evidence of an increase in CVD risk biomarkers.

It is notable that Unwin's group has incorporated LCD guidance in their treatment of patients with type 2 diabetes and prediabetes for over 6 years, including the de-prescribing of diabetes-related medications [168,213,216,217]. These clinicians have reported the safety and efficacy of the LCD, with statistically significant improvements in their patients for weight, HbA1c, lipid profiles and blood pressure.

Although weight loss typically occurs in response to an LCD, improvements in atherogenic dyslipidemia are primarily a result of carbohydrate restriction, rather than weight or fat loss, per se [172,199,218,219]. The consistent and often dramatic improvement in these biomarkers in response to LCDs is strong support for the view that carbohydrate restriction, independent of weight loss, lowers CVD risk.

The basis of the diet-heart hypothesis is the great concern that consumption of food rich in saturated fat would increase risk for CVD. However, in an RCT by Volek et al.[189], subjects in the LCD group exhibited superior improvements in CVD risk factors than the LFD group, despite the LCD group having consumed more than three times as much saturated fat as the LFD group. Moreover, Volek et al.[204], Dreon et al.[220], Sharman et al.[201], and Hays et al.[221] all demonstrated that an LCD rich in saturated fat increased LDL size, leading to a dominance of lbLDL, thereby lowering CVD risk. Similar findings were reported by Ebbeling et al.[222], who found that a high saturated fat, LCD improved measures of insulin-resistant dyslipidemia, without affecting LDL-C, when compared to lower saturated fat diets.

In related work, Cole et al.[223] studied the effects of a moderately low carbohydrate (30%), high fat (55%) diet, supplemented with up to 1800 mg/day of cholesterol (from eggs), on serum lipids in FH subjects. These investigators reported that consumption of additional fat and cholesterol, in the context of an LCD, lowered TGs, and raised HDL, while not affecting LDL-C levels. Comparable findings were reported in the DIETFITS weight loss RCT [224]. These investigators reported that LDL-C in subjects on an LCD was stable across a broad range in dietary cholesterol changes from baseline (>500 mg/day) that the participants consumed over 12 months.

These studies, as well as those reviewed by Astrup et al.[18], reinforce the perspective of the cardiologist, Bahl [225], that an overreliance in public health on saturated fat as the main dietary villain for cardiovascular disease has distracted from the risks posed by other nutrients, such as carbohydrates.

In summary, the LCD, independent of the amount of saturated fat in the diet and weight loss, leads to significant improvements in the most robust lipid risk markers for CVD, characterized by reductions in TGs and sdLDL, with associated increases in lbLDL and HDL-C. LCDs also reduce body weight, inflammatory markers, blood pressure, and blood glucose, and increase insulin sensitivity. These findings are summarized in Fig. 2 and in our recent reviews [48,226].

Given that elevated LDL-C may occur for individuals on an LCD, concerns have been raised that the diet may therefore increase CVD risk. These concerns have been expressed despite a paucity of evidence that total LDL-C is a reliable CVD risk factor. In contrast, there is extensive evidence regarding the efficacy of carbohydrate reduction to improve the most reliable CVD risk biomarkers, such as hyperglycemia, IR, inflammation, hypertension, body weight, and the atherogenic dyslipidemia risk triad. The LCD is also effective at ameliorating components of metabolic syndrome, itself a significant CVD risk factor. While the improvements in these biomarkers support the argument in favor of the CVD benefit of LCDs, it remains that they are surrogate markers only. That is, as surrogate markers they do not provide conclusive evidence that an LCD, with an associated increase in LDL-C, will result in a beneficial effect on hard coronary events, such myocardial infarction or coronary death.

The relative degree of uncertainty as to the outcomes of an LCD-induced elevation of LDL-C raises the question as to whether HMG CoA reductase inhibitor therapy (statins) is indicated for those on an LCD. This question takes on more significance in the context of increasing popularity of different LCDs, including assisting in the management of obesity and diabetes, both representing significant cardiovascular risk factors themselves. Despite the popularity of LCDs, we are aware of no published clinical trials involving subjects with high LDL-C on an LCD, or of trials on subjects on an LCD with statin treatment, with an assessment of hard coronary outcomes. Therefore, it cannot be stated with certainty whether a patient should be concerned about high LDL-C on an LCD, and whether a patient with high LDL-C on an LCD would benefit from statin treatment.

With the caveat of this uncertainty explicitly stated, findings from two RCTs provide guidance as to whether people with a typical LCD biomarker profile (high HDL/low TGs) with high LDL-C, are at increased risk of experiencing a coronary event, and whether they may benefit from statin therapy.

The first RCT was based on a reanalysis of the 4S trial [35], which was a secondary CVD prevention trial in men and women with a history of angina pectoris or acute myocardial infarction. The reanalysis of the 4S trial assessed hard coronary events in placebo or statin treated subjects, all of whom had elevated LDL-C, with either an atherogenic lipid profile (high TGs/low HDL) or a nonatherogenic lipid profile (low TGs/high HDL) [227]. The first finding of importance is that within the placebo group, individuals with an LCD-like (nonatherogenic) lipid profile had a lower incidence of coronary events than placebo-treated individuals with an atherogenic lipid profile (Fig. 3). This finding indicates that the presence of an atherogenic lipid profile, independent of LDL-C, provided a reliable indication of the risk of coronary events in untreated individuals.

The second finding of the 4S reanalysis was that statin treatment produced a significant reduction of coronary events only in those subjects with the atherogenic lipid profile. By contrast, statin treatment produced no significant benefit in those subjects with an LCD-like (nonatherogenic) lipid profile (Fig. 3). That is, despite statin treatment reducing LDL-C to an equivalent level in those with an atherogenic and nonatherogenic lipid profile, only the group with a baseline atherogenic profile demonstrated a treatment-associated reduction in hard coronary events. This finding supports the view that individuals on an LCD with high LDL-C and a nonatherogenic lipid profile (low TGs/high HDL-C) would not benefit from statin therapy.

A second RCT provides findings complementary to the 4S posthoc analysis. The prospective study of Pravastatin in the elderly at risk (PROSPER) study [228] enrolled elderly men (aged 7082 years) with preexisting vascular disease or who were at increased risk of CVD because they had hypertension, diabetes, and/or were smokers. The men were administered pravastatin or placebo, and then assessed for fatal and nonfatal coronary events over 3 years. What is noteworthy is the apparent influence of HDL-C levels on coronary events in the placebo and statin-treated groups. Subjects on the placebo with low HDL-C (<43 mg/dl), consistent with IR, and an atherogenic lipid profile, developed a significantly greater incidence of coronary events than placebo subjects with high HDL-C (>53 mg/dl), independent of their LDL-C levels. This first observation demonstrates that the HDL-C level is a superior indicator of CVD risk than is LDL-C in untreated individuals.

The second observation from the PROSPER study is that benefits of statin treatment occurred only for those subjects with low HDL, independent of their LDL-C levels (Fig. 4). As the authors noted Variation in baseline LDL concentrations did not relate to risk of a coronary event or treatment efficacy. Benefit was predominantly in the lowest tertile of HDL-cholesterol . With low HDL-C being a feature of atherogenic dyslipidemia, this finding is consistent with the 4S reanalysis, and provides additional support for the notion that those with high LDL-C and a nonatherogenic lipid profile (low TGs/high HDL-C) are unlikely to benefit from statin therapy.

The absence of a relation between LDL-C and coronary event reduction with statin treatment suggests that it is their pleiotropic, for example, anti-inflammatory and anticoagulant, effects [229238], rather than LDL-C reduction, per se, that results in a relatively small reduction in coronary events and mortality. Therefore, a person on an LCD with a nonatherogenic lipid profile (low TGs/high HDL-C) is more likely to experience the adverse effects of statins [239252], including an increased risk of new onset type 2 diabetes [246,253258], an increase in fasting blood glucose in patients with and without diabetes [259], mitochondrial dysfunction [260262], tendinopathy [263], myopathy [264,265], acute kidney injury/renal failure [266268] and cognitive deficits [247,269276], than benefits.

We have addressed concerns regarding high LDL-C in individuals on an LCD, which began 5 decades ago and persist to the present day. Our review has evaluated whether these concerns are justified based on three levels of analysis. First, critics of the LCD have focused on how the diet may increase LDL-C. However, there is a substantial literature demonstrating that LDL-C is of limited utility as a CVD risk factor. Second, we reviewed the literature on LCD improvements in CVD risk factors which are superior to LDL-C, such as IR, hypertension, hyperglycemia, LDL particle subtypes, and metabolic syndrome. Third, we summarized RCTs which demonstrate that individuals with high LDL-C and an LCD-like lipid profile (low TGs and high HDL-C), had a low rate of coronary events under nontreatment conditions and derived no CVD benefit from statin therapy. Therefore, our review of the literature provides support for the conclusion that LDL-C reduction with a statin would not provide any benefit in primary or secondary prevention of CVD for an individual on an LCD.

None.

The open access publication cost was provided by the Duke University Research Fund.

There are no conflicts of interest.

Papers of particular interest, published within the annual period of review, have been highlighted as:

of special interest

of outstanding interest

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Statin therapy is not warranted for a person with high... : Current Opinion in Endocrinology, Diabetes and Obesity - LWW Journals

Jay Cutlerrose to the top of bodybuilding during the 2000s after years of building that championship physique. The four-time Olympia champion has been vocal about all things bodybuilding since retiring from action. This includes diet plans that athletes, in and out of bodybuilding, have been adhering to.

Cutler broke the eight-year streak of Olympia victories for Ronnie Coleman in 2006. This was the first of two back-to-back reigns for Cutler, having also won in 2007 and again in 2009-2010. Cutler had an incredible work ethic on stage, epic chest workout routines and dedication to his diet.

During his career, Cutler used to eat upwards of 140 egg whites per day. This is an example of the wild diets he used to follow in order to keep his physique at the highest level. Now, he continues to help others when putting together what might work for them.

The biggest question I get is overcoming challenges, setting goals, how to prioritize, how to stay motivated because they want to build muscle and they want to lose body fat at the same time, can you do this? Yes.

Everyones body is different so its hard for someone to coach someone exactly because they have their own ways.

Jay Cutler broke down some different diet ideas on a recent episode ofJayWalking.Today, Cutler believes that being lean is the preferred look.

I think its better now in todays society, they want to be a lot leaner. Theyre scared to be bigger. I think big is kind of out. Im not sure what you think. I dont know if its in, because Open is still the king. Open is still the king. Its just that the road to get there is much longer. I dont know if its harder.

Back in my early era with bodybuilding, everyone wanted to get bigger. Bigger was like I think people still want to get bigger somewhat, but people were always trying to get bigger.

Jay Cutler explains how all bodies are different, which means that diets have to be put together in different ways. There is no specific way to explain to someone how to diet.

The requests that come in are crazy, the weight challenges for people. It just sucks because the education is just not there for the younger generation. Like, okay this is how you should eat.

Jay Cutler continues to discuss goals that are popular nowadays. Whether it is bulking or curing down, it is important to understand what your plan is when putting together a diet plan.

Whats the goal though? Is it bulking or is it getting lean? I mean, everyones goal is different.

Im suggesting right now, go chase the lean physique. If I was to train someone, and they were bulky, I hate that word bulky but if they had a little more body fat, I would tone them down more before I really started feeding them a lot of calories.

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Jay Cutler Thinks Big Is Out, Prefers Lean Diet: They Want To Be A Lot Leaner - Generation Iron Fitness Network

Disease killed more men during the American Civil War than combat, accounting for more than half the 600,000 fatalities during the conflict. Dysentery and its accompanying diarrhea alone were responsible for an estimated 100,000 deaths, reportsHistoryNet. Poor diet was one of the causes of this, per Smithsonian Magazine, and Dr. Salisbury, by this time a physician for the Union Army, believed he had a solution. His prescription was lean minced beef formed into patties, which he gave to soldiers to improve their nutrition and digestion.

Dr. Salisbury's description of his steak is a rather unappetizing one: "muscle pulp of beef." (via Smithsonian Magazine) Over time, its actual makeup would be codified by the U.S. Department of Agriculture, which notes in its Food Standards and Labeling Policy Book that Salisbury steak must be at least 65% chopped meat, of which no more than 25% of that may be pork. The rest should be beef, with no more than 30% fat allowed in total. Liquids such as milk and cream may also be used, undoubtedly in the brown gravy.

The chopped beef patties in Salisbury steak were closely related to hamburgers, of course, but it took another war to promote the differences. During World War I, anti-German sentiment led the U.S. Army to eschew hamburgers in favor of the Salisbury steak, which it served to troops, according to the William G. Pomeroy Foundation.

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Salisbury Steak's Historic Connection To The Civil War - Tasting Table

LOS ANGELES As USC players took turns sitting around fold-out tables at media day last week, each one seemed to have their own off-season accomplishments to brag about.

I lost six pounds of fat, gained five pounds of muscle, center Brett Neilon reported.

I was at like 10 [percent body fat] last year, rush end Korey Foreman said. Now Im going into five.

The man at the center of these developments and the off-season regimen for USC is strength and conditioning coach Bennie Wylie.

Wylie was always a key part of head coach Lincoln Rileys vision for USC. After spending four seasons together at Oklahoma, Wylie literally joined Riley on the private plane from Norman to Los Angeles without a contract, ready to leave his mark on the Trojans new era.

After spending January and February readying the roster for spring camp, Wylie prepared off-season regimens for the roster. In addition to the traditional weight and conditioning work, Wylie had the Trojans doing sprinting and cutting and hand-to-hand combat that players likened to wrestling.

Quickly, Wylie and his team of staffers have earned the trust of the USC locker room.

The strength staffs elite and theyre professional, Neilon said. A lot of us got bigger, stronger and faster. The numbers and the outcomes are there. [Wylie] trains us like professional athletes and he takes care of guys, too.

In addition to the actual workouts, Wylies team has developed diets to help players hit their weight and body fat goals.

It was just being able to adapt to whats best for us, said Foreman, who cut out fried foods at Wylies behest, because at the end of the day they have our best interests.

And Wylie gives time to provide special attention to injured players and make sure they dont fall behind even as they sit out the full teams workouts.

Soon after a diagnosis, Wylie has turned up with an updated regimen specific to a player and his new limitations.

Usually when a guy get hurt, they dont work out. Youre gonna work out with Coach Wylie, tight end Malcolm Epps explained. Theres some part of your body that works, and hes gonna work it out.

But after the off-season work, there have been fewer injuries for USC to report than in past training camps. Sure there are players on the sidelines; tight end Jude Wolfe was in a walking boot during Mondays practice, while defensive backs Jaylin Smith and Latrell McCutchin were in street clothes with what Riley described as bumps and bruises.

But for the most part, USC has had a clean bill of health, and a new look, in Rileys opinion.

Weve taken several steps since spring, Riley said after the first day of camp. I think the biggest thing I notice right now is a lot of our bodies are starting to change in a way they need to change. You see a little more pop, a little more speed, a little more physicality.

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USC feeling the benefits of new off-season regimens - The Whittier Daily News