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Smoked Salmon and Chive Soufflé Omelette

Ingredients

150 ml milk
1 small onion, sliced
1 small carrot, sliced
1 clove
1 bay leaf
250 g smoked salmon
75 g butter
1 tablespoon plain flour
3 large eggs, separated
6 tablespoons sour cream
4 tablespoons chopped fresh chives
2 tablespoons freshly chopped parsley
2 tablespoons freshly grated Parmesan cheese
salt and freshly ground black pepper

Method

1. Put the milk in a saucepan, add the onion, carrot, clove and bay leaf, heat until almost boiling, then turn off the heat and let stand for 10 minutes.
2. Add half the smoked salmon, then simmer for 5 minutes until opaque.
3. Remove the fish to a plate and flake it with a fork. Strain and reserve the milk.
4. Melt half the butter in a small saucepan, stir in the flour, gradually whisk in the reserved milk and bring to the boil, stirring all the time until thickened. Remove from the heat.
5. Put the egg yolks and half the sour cream in a bowl, beat well, then stir into the sauce. Add salt and pepper to taste.
6. Carefully stir in the cooked smoked salmon and the chives and parsley.
7. Whisk the egg whites in a second bowl until stiff but not dry, then fold into the sauce.
8. Melt the remaining butter in an omelette pan and pour in the salmon mixture. Cook over a medium heat until just beginning to set, then scatter over the remaining smoked salmon on spoon over the remaining sour cream.
9. Carefully flip one half of the omelette over to cover the salmon. Scatter with Parmesan and finish off in a preheated oven at 200°C (400°F) for 5 minutes. Serve immediately, straight from the pan.

Makes 2 servings.

Source: Salmon

Food as a Hormone

Enlarge image . . . . .

Karen K. Ryan and Randy J. Seeley wrote . . . . . . . . .

Diet has an enormous impact on many aspects of our health, yet scientific consensus about how what we eat affects our biology remains elusive. This is especially true with respect to the ongoing debate about obesity. While many in the scientific community focus on how high-fat diets can lead to increased body weight (1), others assert that we should blame processed carbohydrates (2). Is it possible that this focus on macronutrients (i.e., fats, proteins, and sugars) is misplaced?

Much of the recent public discourse about the interaction between food and metabolic health relies on two basic approaches (see above figure). One is nutritional epidemiology, in which populations of people who eat different foods are compared with regard to indices of health such as body weight, with a goal of determining which diets are more or less “healthy.” The other is biochemistry, in which the goal is to determine how different macronutrients are processed to yield energy. Despite valuable information provided by these two approaches, neither has resulted in a translatable scientific basis for recommending diets that improve metabolic health or reduce body weight for a large percentage of the affected population, perhaps because considering food only in terms of its macronutrient content overlooks the complexities of how food interacts with our bodies.

Nutritional epidemiology and biochemical approaches, focusing primarily on the relationship between macronutrient consumption and metabolic outcomes, have not provided a translatable scientific basis to recommend diets that improve metabolic health for a broad range of people. Alternatively, understanding our diets as a collection of signaling molecules, having hormone-like actions via cell-surface and nuclear receptor signaling, may provide new insights into the relationship between what we eat and metabolic disease. Moreover, this framework may eventually allow us to make dietary recommendations from the bottom up—based on the ability of specific foods to alter relevant signaling pathways.

A growing body of evidence suggests an alternative perspective. That is, circulating substrates derived from food have specific direct and indirect actions to activate receptors and signaling pathways, in addition to providing fuel and essential micronutrients. Ultimately food can be considered as a cocktail of “hormones.” A hormone is a regulatory compound produced in one organ that is transported in blood to stimulate or inhibit specific cells in another part of the body. Hormones exert their effects on target tissues by acting on cell-surface receptors to alter activity through intracellular signaling cascades or via nuclear receptors to regulate gene transcription. Although food is not produced in the body, its components travel through the blood, and nutrient substrates can act as signaling molecules by activating cell-surface or nuclear receptors.

As an example, nutritional epidemiology has touted the benefits of eating omega-3 fatty acids to protect against cardiometabolic syndrome and weight gain (3). Yet simple biochemistry cannot satisfactorily explain why omega-3 fatty acids should lead to benefits compared to other fatty acids. Omega-3 fatty acids bind to and activate the cell-surface receptor GPR120 (4), which is expressed in important metabolic tissues including adipose tissue and muscle. Reduced GPR120 signaling is associated with inflammation, weight gain, and impaired glucose control in both mice and humans (4, 5). Thus, to generate the full spectrum of beneficial effects on vascular disease risk, ingested omega-3 fatty acids are not simply processed to generate energy, but additionally act via GPR120 in key tissues to improve metabolic endpoints.

Whereas activating GPR120 appears to protect against weight gain, other lipid-activated receptors exert the opposite effect. Peroxisome proliferator–activated receptor γ (PPARγ), for example, is a nuclear receptor that is activated by a variety of fatty acids and regulates transcription of genes important for lipid and glucose metabolism. Increasing PPARγ activity with pharmacological agonists enhances lipid storage in adipose tissue, and also acts in the brain to cause hyperphagia, dual actions that promote accretion of body fat (6– 8). Consistent with this, reducing PPARγ activity in the brain decreases consumption of high-fat diets, thereby blunting weight gain (6, 8). These studies lay the groundwork for understanding how components of high-fat diets cause overconsumption and weight gain by activating specific fatty acid receptors in the brain.

In addition to acting directly on these specialized fatty acid receptors, there is evidence that some dietary fatty acids also modify the actions of classical hormones. For example, the stomach-derived hormone ghrelin increases food intake and weight gain by binding to its receptor, growth hormone secretagogue receptor (GHSR). However, for ghrelin to signal effectively, a fatty acid must first be attached to the peptide as a side chain. Different fatty acid side chains derived from different dietary fats change the ability of ghrelin to increase food intake (9). These fatty acid side chains come from ingested food rather than from adipose tissue (10). In this way, specific dietary components can exert hormone-like metabolic effects by physical interaction with a peptide hormone.

Fatty acids are not the only direct source of “hormones” in our food; certain amino acids can also activate signaling pathways. The most-studied are the branched-chain amino acids including leucine, which activates the mammalian target of rapamycin (mTOR) pathway. mTOR is a serine-threonine kinase that regulates cell-cycle progression, growth, and insulin action (11). Leucine directly activates the mTOR pathway in the central nervous system to reduce food intake and body weight (12, 13).

Food components also interact with gut flora to induce indirect signaling cascades within the body. For example, nondigestible complex carbohydrates, including dietary fiber, are metabolized by the gut microbiota and fermented to short-chain fatty acid (SCFA) end products—mainly acetate, propionate, and butyrate (14). These SCFAs bind to and activate cell-surface receptors free fatty acid receptor 2 (FFAR2) and FFAR3 to alter host metabolism. For example, FFAR2 and 3 are expressed on entero-endocrine L cells that produce the incretin hormone glucagon-like peptide–1 (GLP-1). Stimulation of L cells with SCFA induces GLP-1 secretion, but this effect is diminished in the absence of FFAR2 or, to a lesser extent, FFAR3 (15). Acetate and propionate also activate FFAR2 on adipocytes to increase expression of the weight-reducing hormone leptin. In this way, specific dietary carbohydrates, modified by the gut microbiota, can signal at specific receptors to alter whole-body energy and glucose metabolism.

Viewing food as a hormone could substantially influence how we make dietary recommendations to promote health or treat specific diseases. Rather than using only nutritional epidemiology to identify what healthy people consume, we may be able to design diets from the bottom up—based on their ability to alter signaling pathways in specific tissues that we know are linked to metabolic disease. In addition, this framework suggests that the argument over whether fat or sugar is to blame for the increasing incidence of obesity may be misguided. Macronutrients are classified by their energy-yielding biochemical properties, not by their ability to activate receptors in a manner similar to that of a hormone. It may be more productive to examine the signaling properties of a given diet to understand whether it will promote weight gain or weight loss. Identifying these food- and food metabolite–receptor interactions will provide new opportunities to understand the relationship between what we eat and diseases including obesity.

Source: U.S. National Library of Medicine

Many Misdiagnosed With Multiple Sclerosis

Almost one in five multiple sclerosis patients may be misdiagnosed with the autoimmune disease, according to a new study.

Of 241 previously diagnosed multiple sclerosis (MS) patients referred to two major Los Angeles medical centers for treatment, nearly 18% did not actually have the autoimmune disease, the researchers found.

Those patients spent an average of nearly four years being treated for MS before receiving a correct diagnosis, the study authors said.

“I’ve seen patients suffering side effects from the medication they were taking for a disease they didn’t have,” said study leader Dr. Marwa Kaisey, from Cedars-Sinai Medical Center in Los Angeles.

“Meanwhile, they weren’t getting treatment for what they did have. The cost to the patient is huge — medically, psychologically, financially,” Kaisey said in a Cedars-Sinai news release.

The most common correct diagnosis among the patients misdiagnosed with MS was migraine (16%), followed by radiologically isolated syndrome, a condition in which patients do not experience symptoms of MS even though their imaging tests look similar to those of MS patients.

Other diagnoses included nerve damage and a disorder of the vertebrae called spondylopathy, the findings showed.

Among the patients misdiagnosed with MS, 72% had been prescribed MS treatments. Of those, 48% received therapies that can carry the risk of a viral infection-caused disease in the white matter of the brain (progressive multifocal leukoencephalopathy).

The researchers estimated that the unnecessary treatments given to the misdiagnosed patients in this study alone cost nearly $10 million.

“The diagnosis of MS is tricky. Both the symptoms and MRI testing results can look like other conditions, such as stroke, migraines and vitamin B12 deficiency,” Kaisey explained.

“You have to rule out any other diagnoses, and it’s not a perfect science,” she added.

The study was published in the journal Multiple Sclerosis and Related Disorders.

“The first step, which is what we’ve done here, is to identify the problem, so now we’re working on potential solutions,” Kaisey said.

Source: HealthDay

Five Ways to Move More at Work and Make It Count

With the recent news that even small bouts of exercise lead to significant health benefits, the American Heart Association, the leading voluntary health organization devoted to a world of longer, healthier lives, is urging adults to move more and make it count where they spend most of their time – at work.

“It doesn’t matter whether you get activity in short bursts of a few minutes or longer periods of time,” says Eduardo Sanchez, M.D., M.P.H., FAAFP and American Heart Association’s chief medical officer for prevention. “Any activity – even small, short bouts – will provide a health benefit. If you have been totally inactive and start exercising, you will benefit. But even if you’re already active, adding more movement adds even more benefit.”

Most adults spend the majority of their waking hours at work and find themselves with little time or energy left at the end of the day to exercise. Experts say those who struggle to carve out time for a separate workout should use any opportunity to sneak in physical activity throughout the day. Focusing on moving more and sitting less throughout the day can help – there is benefit to any physical activity regardless of the length of the activity.

For adults, the American Heart Association recommends at least 150 minutes per week of moderate activity or 75 minutes of vigorous activity, or a combination of those activities, such as such as brisk walking, yoga or gardening. In addition, the Association recommends two days per week of moderate- to- high intensity muscle strengthening activity, such as running, jumping rope or swimming laps.

April, known as Move More Month, is an opportunity to examine personal habits and strive to incorporate additional daily activity.

The month of April, with its reputation for renewal and growth, is the perfect time to examine your personal exercise routine and make any adjustments needed. Move More Month can help you get started on the right path and is a good reminder that small choices to move more daily, add up to better your health.

Here are some ideas to incorporate more movement into the work day from the American Heart Association’s Healthy for Good™ initiative:

• Take a walk on your lunch break. Don’t focus on the step count or the minutes, just move more when your schedule allows.
• Increase your activity in simple ways around the office. Take the stairs instead of the elevator, park farthest from the door in the parking lot, convert conference room meetings to walking meetings or get up and walk to someone’s desk instead of sending email.
• Schedule exercise on your calendar. Add exercise to your calendar and treat your scheduled time like an important meeting.
• Find a partner. Having a partner to keep you accountable and motivated can be the key to keeping your healthy habits moving forward.
• Take advantage of workplace wellness offerings. Ask your supervisor or human resources department what employee wellness resources and incentives are available.

Starting a journey to be more active at work can inspire colleagues and lead to a healthier workplace in addition to boosting personal health and wellbeing.

Source: American Heart Association

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