A.Blood

B.Oxygen

C.Glucose

D.High energy ATPs

E.Free fatty acid

Answer : A  will be considered  by most , as  correct answer .  A can provide B to E . But it is also a fact heart can survive without  A.  

                    Myocardium requires energy first  ! it does not in fact bother about from where it is coming at the time of crises.It may be right if you restore the coronary blood flow all other components (B-E) are made available to the heart . 

                   The heart can survive off  the coronary circulation with only chemical support during cardiac surgery and also a during  heart transplantation  explanted  donor heart survives on a ice box during transit and till it is transplanted into the recipient heart

                    But ironically we spend much of our energy and efforts in restoring blood flow.One need to spare a thought about the quality of blood also . This is especially important  in the setting of ischmia  where a  metabolic centric approach will add further benefit.

Energy based approach to ischemia : Is it relavent ?

                                              Heart is a fascinationg mechano biological organ  pumping   millions of  gallons of blood  .Fuel for this is self genertated  on a continuous basis  from the circulation blood .So  the key to human survival is the coronary blood flow that supplies the fuel and nutrients to the heart. When this key supply line is under threat  during  acute coronary syndrome cardiologist have  the only option of restoring the compromised blood supply by any means . But during chronic ischemia there is  no  urgency. There has always been an option of enriching the  blood with energisers like ATPs,  glucose,  hemoglobin etc .Providing energy support to the failing heart has never captured the imagination of cardiac physicians until recently.Still most are skeptical about  the concept of biochemical ischemia.

Click to download full PPT presentation

Metabolic manipulation of  CAD( Will be available shortly)

(Healthy Back institute Newsletter) When it comes to blood sugar, the closer you can keep it in the normal range of 80 to 89 mg/dL, the better.

For years I've been warning that blood sugars even in the 90 to 100 range show that you are becoming insulin resistant and on your way to diabetes.

A recent study of 47,000 Kaiser Permanente patients validated this observation.

The study, published in the American Journal of Medicine, found that blood sugar, blood glucose (BG) levels in the 95-99 range, more than doubled a person's risk of becoming diabetic.  In fact, for every point over 85 mg/dL the risk of becoming diabetic increased 6%, even when they controlled for other factors.1

Accordingly, the study noted that there was more incidence of cardiovascular disease and hypertension in those with higher BG.  Why is this research so important?  It flies in the face of currently accepted medical guidelines that for years have used 100 as the magic number for diagnosing "pre-diabetes."

At LMI, I've been seeing red flags for years when patients come in with BG levels even in the 90s, because these levels are often accompanied by being somewhat overweight, having a thick waist, or the spare tire of dangerous belly fat. These are signs that the body can no longer efficiently process the sugars that come from complex carbohydrates in whole grains, starchy vegetables, fruits, and simple sugars.

In other words, they are signs of insulin resistance. Insulin is the "key" that unlocks the door to each cell in the body, letting glucose into the cell to be processed for energy.  If the insulin key is faulty, the glucose remains in circulation, raising triglycerides, lowering HDL, and usually ending up at the waistline.

Anytime you see your doctor for a routine physical, fasting blood glucose is tested along with other blood labs.  If your blood sugar comes in less than 100 mg/dL, you will likely get an "all clear," when it comes to diabetes risk.  If you're overweight, have elevated blood pressure and are sedentary - other risk factors for insulin resistance - your doctor may suggest you lose a few pounds and add a few days of walking to your weekly routine.

But typically that won't happen unless your blood sugar levels come in greater than 100 mg/dL, but less than 126 mg/dL - the pre-diabetes range - then you will get a more stern warning regarding diet and exercise.  However, it's not until your fasting blood sugar levels reach over 126 mg/dL that you are diagnosed with type II diabetes or non-insulin dependent diabetes.

By the time you get the "true diabetes" diagnosis - your body is so insulin resistant that it may need much more than the "diabetic diet" and a walking routine to get your blood sugar levels under control.  This is when you may need an oral hypoglycemic medicine, which comes with a nice little set of nutrient-depleting side effects.

Wouldn't it be nice if your doctor had warned you of your increased risk way before you even reached the 100 mark for blood glucose?  For years, I have been warning my patients that blood sugar over 90 is a sign they are becoming insulin resistant.  But because medical guidelines give an "all clear" at anything under 100, too many patients don't want to believe they could be at risk - even with fasting BGs of 98 and showing every sign of insulin resistance.

At LMI, we go to work on the insulin resistance by giving our patients blood sugar support nutrients like chromium and having our dietitians provide instruction on a lower carb diet.  Ironically, we sometimes receive calls from their primary care physicians questioning our course of action because they think these patients "are fine." But our philosophy is, don't wait to become diabetic - take action well ahead of time.

Hopefully, the medical community's eyes will open after reading the newly published article in the American Journal of Medicine. This phenomenal research has hit the nail on the head and may finally spur new guidelines to be issued for the management of blood sugar. Medical news can take a while to trickle down into actual practice, so in the meantime, you may need to become more proactive on your own.

If your blood work reveals a high-normal fasting blood sugar level, cut down on carb-heavy sugars, starches, and fruits, up the organic vegetables and proteins, and get your body moving.  You may be saving yourself from becoming a diabetes statistic.

Reference

1.    Am J Med. 2008;121:519-524

[Ed. Note: James LaValle, R.Ph, ND, CCN, is the founding Director of the LaValle Metabolic Institute, one of the largest integrative medicine practices in the country.  He was named as one of the 50 most influential pharmacists in the US by American Druggist magazine.  Dr. LaValle is the author of more than a dozen books including the bestseller, Cracking the Metabolic Code: 9 Keys to Optimal Health.

[This is NOT an endorsement of any services or products of the LaVelle Metabolic Institute, of which I have no affiliation. It is merely an acknowledgement of the writer and the contents of his article.]

Zitat: So mancher bekommt nämlich einen höllischen Schreck, wenn er in den Spiegel oder auf die Anzeige der Waage schaut. Lustvolles All-Inklusive-Schmausen hat seine Spuren hinterlassen. Geht es Ihnen auch so? Dann ist Abnehmen angesagt.

Oder wollen Sie dem beleibten Weihnachtsmann in diesem Jahr Konkurrenz machen und im nächsten Sommer so an den Strand? Jetzt nur keine schlechte Laune bekommen, sondern gezielt handeln. xx-well.com weiß, wie Sie die Pfunde schnell wieder loswerden.

Abnehmen mit dem Online-Diätcoach von xx-well.com: Abnehmen ohne Jojo-Effekt mit dem Diätcoach von xx-well.com. Beste Noten von Stiftung Warentest. - viele haben es bereits geschafft und sich damit einen lang ersehnten Traum verwirklicht.

Zitate: Magenta Arnold-Nickel (52): "Ausschlaggebend war die Bemerkung eines Taxifahrers, der sich einfühlsam erkundigte, wann es denn mit der Entbindung soweit sei. Im Internet habe ich xx-well gefunden und es hat geklappt. Ich habe bereits 19 Kilo abgenommen. Bei 20 Kilo gibt es online und offline ein Gläschen Champagner."

Sabine Alipour (38): Am besten hat mir die Community geholfen. Dort trifft man Leute in ähnlicher Lage. Man motiviert und unterstützt sich gegenseitig. Nach etwa 10 Monaten hatte ich über 20 Kilo abgenommen."

Martina Rüdiger (42): "Mit xx-well bekam ich das Bewusstsein für die Menge der Nahrungsaufnahme zurück. Die größte Hilfe dabei war das Protokollieren der Nahrungsmittel und Getränke und der Überblick über die Nährwerte. So habe ich 10 Kilo abgenommen!"

Was bietet der Coach?
Er hat täglich jede Menge lecker-leichte Rezeptideen.
Er weiß immer, wie es mit Ihrer Nährstoffbilanz aussieht.
Er erstellt Grafiken, die Ihren Diätverlauf auf einen Blick zeigen.
Er kennt alle Tricks zum Durchhalten.
Er lässt Sie nicht allein und hat Antworten auf all Ihre Fragen.
Er erstellt einen individuellen und effektiven Fitnessplan.
Er zeigt Ihnen, wie Sie im Alltag ganz leicht "anders" zu essen lernen.
Er lässt Sie nicht hungern.
Er bringt Sie, so schnell es geht, zum Erfolg.
Er wurde von der Stiftung Warentest mit "uneingeschränkt empfehlenswert" bewertet.

Oder wie wäre es alternativ zum klassischen Online-Diätcoach mit dem BRIGITTE-DIÄT-Coach. xx-well und BRIGITTE haben ein einzigartiges Produkt geschaffen, das die erfolgreichen BRIGITTE-Rezepte, die schon vielen tausend Frauen das Schlankwerden erleichtert haben, mit den Fähigkeiten eines Personal Trainers kombiniert.

Zitate: Helga Klein (46): "Von Kleidergröße 52 bin ich auf 42 geschrumpft, habe eine völlig neue Garderobe. 34 Kilo weniger - danke für mein neues Leben."

Julia Jonas (36): "Ich brauche in meinem Tagesablauf Flexibilität. Das bot mir der Coach. Sportprogramm und Speiseplan wurden individuell zusammengestellt. Ich konnte meine Diät nach meinem Timing durchführen - und habe schließlich 8 Kilo verloren."

0,1 % Fett - Tappen Sie nicht in die Zuckerfalle

Light-Joghurt, Gummibärchen ohne Fett, Lakritz ohne Fett - super, was es da seit neuestem alles gibt. Das erleichtert das Vorhaben schlank zu bleiben oder Pfunde zu verlieren ungemein. Und ein gutes Gewissen machen diese Produkte auch. Schließlich ist es gesund, Fett einzusparen und unnötige Kalorien zu vermeiden. Tja, schön wär‘s, doch die Sache hat einen Haken. Diese Nahrungsmittel sind weder ein kulinarischer Freifahrtschein noch die Ideallösung. Der Grund hat einen Namen, und der lautet Zucker.

Viele Packungsangaben verwirren, versteckte Dickmacher werden nicht erkannt. Denn die Angabe 0,1 % bei einem Joghurt beispielsweise sagt nur aus, dass der Fett-Anteil sehr gering ist. Gleichzeitig kann der Zucker- und damit der Kaloriengehalt aber sehr hoch sein. Denn nicht nur Fett macht Fett. Auch Zucker wandelt der Körper in Fettpölsterchen um.

Auch Gummibärchen oder Lakritz werden mit dem Zusatz "ohne Fett" beworben. Es stimmt zwar, dass sie fast kein Fett enthalten, dafür aber jede Menge Zucker. In drei Gummibärchen steckt fast ein Stück Würfelzucker. Das bedeutet: Der Marketing-Trick von vielen Süßwarenherstellern "kein Fett und deshalb nicht dick machend", ist Unsinn.

Aber wenn Zucker drin ist, würde das doch auch draufstehen? Ja, aber erstens guckt danach keiner mehr, wenn die Aufschrift "nur 0,3% Fett" einen verlockend anlächelt. Zweitens sind viele Menschen in dem Irrglauben, dass nur Fett fett macht und drittens sind die Zuckerangaben auch "gut versteckt".

Oder wussten Sie, dass Zucker unter ganz verschiedenen Namen in der Zutatenliste auftauchen kann ( z.B. Glucose(sirup), Fructose, Dextrose, Invertzucker(sirup), Fruchtsüße) und zu der ansonsten so gesunden und Energie spendenden Gruppe der Kohlenhydrate zählt? Steht also auf einer Lebensmittelverpackung die Angabe "19 Gramm Kohlenhydrate", kann man häufig kleingedruckt darunter lesen, dass davon 19 Gramm Zucker sind.

Wie also lautet das Fazit? Wie immer: Die Menge macht’s. Joghurt ist gesund, ein paar Gummibärchen oder Lakritz sind vollkommen in Ordnung. Man sollte es nur eben nicht übertreiben, weil man sich durch irreführende Angaben fälschlich auf der sicheren und damit kalorienarmen Seite fühlt.

Tool des Monats: Workout Week

Sie wollten schon immer Ihren Rücken für eine stolze Haltung stärken, die "Last" von Schultern und Nacken nehmen und sich mehr um die Problemzone Nummer eins - den Bauch - bemühen? Dann sind Sie hier genau richtig.

xx-well bietet Ihnen gezielte Trainingsvorschläge für die verschiedenen Muskelpartien. Entscheiden Sie, welchen Bereich Sie trainieren möchten, und Sie werden insgesamt sieben videogestützte Übungen erhalten. Sie fürchten eine Über- oder gar eine Unterforderung, da die Übungen nicht individuell auf Sie zugeschnitten sind? Kein Problem, einfach gleich zu Beginn zwischen Anfänger und Fortgeschrittenen wählen und schon ist die passende Trainingsanforderung gewährleistet.

Interessiert? Dann klicken Sie sich zum xx-well Tool des Monats. Zum Anbieter:
Abnehmen ohne Jojo-Effekt mit dem Diätcoach von xx-well.com. Beste Noten von Stiftung Warentest.

In fact, Investigators found that diet and exercise resulted in a 58% reduction in diabetes risk among people who are prime candidates for developing the condition, which is associated with obesity and sedentary lifestyle (The New England Journal of Medicine May 3, 2001; 344: 1343-1350, 1390-1392).

The general North American population is eating more and exercising less, and increasing numbers of adults and children are developing the syndrome, which results when a person loses the ability to use insulin effectively. This syndrome can develop into type 2 diabetes and increase the risk of heart disease if left untreated.

Exercise works by increasing the sensitivity of insulin receptors so the insulin that is present works much more effectively and your body doesn’t need to produce as much. Blood sugar is only the symptom in most diabetics; the real challenge is to control your insulin levels. Once the insulin levels are stabilized it is common for the blood sugar to come back to normal levels.

The orthodox medical community does not put enough emphasis on the powerful value of exercise. Optimum exercise levels in relation to diabetes are just not appreciated or understood enough.

There are three important variables with exercise:

• Length of time
• Frequency
• Intensity

I believe strongly in short and intense duration exercise sessions. Just make sure you have worked up gradually to these though, as you do not want to put undue stress on the body too early. However, researchers say even modest amounts of exercise, without weight loss or loss of abdominal fat, can improve indicators of glucose and fat metabolism among inactive, middle-aged adults, a group that is particularly at risk for developing type 2 diabetes.

Diabetes affects an estimated 18 million people in the US (90 percent to 95 percent have type 2 diabetes) - 13 million have been diagnosed, but 5.2 million are unaware they have the disease. According to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and the American Diabetes Association, those affected include:

• 9.3 million US women (8.7 percent of all women)
• 8.7 million US men (8.7 percent of all men)
• 206,000 people under age 20
• 8.6 million adults over age 60
• 2.7 million African Americans (11.4 percent of all African Americans)
• 2 million Hispanic/Latino Americans (8.2 percent of all Hispanic/Latino Americans)
• 12.5 million Caucasian Americans (8.2 percent of all Caucasian Americans)

According to the most recent statistics, diabetes was the sixth leading cause of death, and the fifth leading cause of death from disease. Diabetes costs $90 billion annually in direct medical costs. Diabetes costs $40 billion annually in indirect costs (loss of work, disability, loss of life) [http://www.northshorelij.com/body.cfm?id=7767]

So get off your duff and get active. It may require some sweat and sacrifice, but the payoff is an increased life expectancy. It's better than a pill and doesn't cost you nearly as much.

In the Kitchen with Mother Linda
The Murky World of High-Fructose Corn Syrup
By Linda Joyce Forristal, CCP, MTA

Think of sugar and you think of sugar cane or beets. Extraction of sugar from sugar cane spurred the colonization of the New World. Extraction of sugar from beets was developed during the time of Napoleon so that the French could have sugar in spite of the English trading blockade.

Nobody thinks of sugar when they see a field of corn. Most of us would be surprised to learn that the larger percentage of sweeteners used in processed food comes from corn, not sugar cane or beets.

The process for making the sweetener high fructose corn syrup (HFCS) out of corn was developed in the 1970s. Use of HFCS grew rapidly, from less than three million short tons in 1980 to almost 8 million short tons in 1995. During the late 1990s, use of sugar actually declined as it was eclipsed by HFCS. Today Americans consume more HFCS than sugar.

High-fructose corn syrup (HFCS) is produced by processing corn starch to yield glucose, and then processing the glucose to produce a high percentage of fructose. It all sounds rather simple--white cornstarch is turned into crystal clear syrup. However, the process is actually very complicated. Three different enzymes are needed to break down cornstarch, which is composed of chains of glucose molecules of almost infinite length, into the simple sugars glucose and fructose.

First, cornstarch is treated with alpha-amylase to produce shorter chains of sugars called polysaccharides. Alpha-amylase is industrially produced by a bacterium, usually Bacillus sp. It is purified and then shipped to HFCS manufacturers.

Next, an enzyme called glucoamylase breaks the sugar chains down even further to yield the simple sugar glucose. Unlike alpha-amylase, glucoamylase is produced by Aspergillus, a fungus, in a fermentation vat where one would likely see little balls of Aspergillus floating on the top.

The third enzyme, glucose-isomerase, is very expensive. It converts glucose to a mixture of about 42 percent fructose and 50-52 percent glucose with some other sugars mixed in. While alpha-amylase and glucoamylase are added directly to the slurry, pricey glucose-isomerase is packed into columns and the sugar mixture is then passed over it. Inexpensive alpha-amylase and glucoamylase are used only once, glucose-isomerase is reused until it loses most of its activity.

There are two more steps involved. First is a liquid chromatography step that takes the mixture to 90 percent fructose. Finally, this is back-blended with the original mixture to yield a final concentration of about 55 percent fructose--what the industry calls high fructose corn syrup.

HFCS has the exact same sweetness and taste as an equal amount of sucrose from cane or beet sugar but it is obviously much more complicated to make, involving vats of murky fermenting liquid, fungus and chemical tweaking, all of which take place in one of 16 chemical plants located in the Corn Belt. Yet in spite of all the special enzymes required, HFCS is actually cheaper than sugar. It is also very easy to transport--it's just piped into tanker trucks. This translates into lower costs and higher profits for food producers.

The development of the HFCS process came at an opportune time for corn growers. Refinements of the partial hydrogenation process had made it possible to get better shortenings and margarines out of soybeans than corn. HFCS took up the slack as demand for corn oil margarine declined. Lysine, an amino acid, can be produced from the corn residue after the glucose is removed. This is the modus operandi of the food conglomerates--break down commodities into their basic components and then put them back together again as processed food.

Today HFCS is used to sweeten jams, condiments like ketchup, and soft drinks. It is also a favorite ingredient in many so-called health foods. Four companies control 85 percent of the $2.6 billion business--Archer Daniels Midland, Cargill, Staley Manufacturing Co. and CPC International. In the mid-1990s, ADM was the object of an FBI probe into price fixing of three products--HFCS, citric acid and lysine--and consumers got a glimpse of the murky world of corporate manipulation.

There's a couple of other murky things that consumers should know about HFCS. According to a food technology expert, two of the enzymes used, alpha-amylase and glucose-isomerase, are genetically modified to make them more stable. Enzymes are actually very large proteins and through genetic modification specific amino acids in the enzymes are changed or replaced so the enzyme's "backbone" won't break down or unfold. This allows the industry to get the enzymes to higher temperatures before they become unstable.

Consumers trying to avoid genetically modified foods should avoid HFCS. It is almost certainly made from genetically modified corn and then it is processed with genetically modified enzymes. I've seen some estimates claiming that virtually everything--almost 80 percent--of what we eat today has been genetically modified at some point. Since the use of HFCS is so prevalent in processed foods, those figures may be right.

But there's another reason to avoid HFCS. Consumers may think that because it contains fructose--which they associate with fruit, which is a natural food--that it is healthier than sugar. A team of investigators at the USDA, led by Dr. Meira Field, has discovered that this just ain't so.

Sucrose is composed of glucose and fructose. When sugar is given to rats in high amounts, the rats develop multiple health problems, especially when the rats were deficient in certain nutrients, such as copper. The researchers wanted to know whether it was the fructose or the glucose moiety that was causing the problems. So they repeated their studies with two groups of rats, one given high amounts of glucose and one given high amounts of fructose. The glucose group was unaffected but the fructose group had disastrous results. The male rats did not reach adulthood. They had anemia, high cholesterol and heart hypertrophy--that means that their hearts enlarged until they exploded. They also had delayed testicular development. Dr. Field explains that fructose in combination with copper deficiency in the growing animal interferes with collagen production. (Copper deficiency, by the way, is widespread in America.) In a nutshell, the little bodies of the rats just fell apart. The females were not so affected, but they were unable to produce live young.

"The medical profession thinks fructose is better for diabetics than sugar," says Dr. Field, "but every cell in the body can metabolize glucose. However, all fructose must be metabolized in the liver. The livers of the rats on the high fructose diet looked like the livers of alcoholics, plugged with fat and cirrhotic."

HFCS contains more fructose than sugar and this fructose is more immediately available because it is not bound up in sucrose. Since the effects of fructose are most severe in the growing organism, we need to think carefully about what kind of sweeteners we give to our children. Fruit juices should be strictly avoided--they are very high in fructose--but so should anything with HFCS.

Interestingly, although HFCS is used in many products aimed at children, it is not used in baby formula, even though it would probably save the manufactueres a few pennies for each can. Do the formula makers know something they aren't telling us? Pretty murky!

About the author

Linda Forristal, CCP, MTA is the author of Ode to Sucanat (1993) and Bulgarian Rhapsody (1998). Visit her website at www.motherlindas.com.

----------------------------------------------------------

This article appeared in Wise Traditions in Food, Farming and the Healing Arts,
the quarterly magazine of the Weston A. Price Foundation, Fall 2001
This page was posted on 12/03/03

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In humans, triglycerides, which are a type of fat in the blood, are mostly formed in the liver. Dr. Parks said the liver acts like “a traffic cop” who coordinates how the body uses dietary sugars. When the liver encounters glucose, it decides whether the body needs to store it, burn it for energy or turn it into triglycerides.

But when fructose enters the body, it bypasses the process and ends up being quickly converted to body fat.

“It’s basically sneaking into the rock concert through the fence,” Dr. Parks said. “It’s a less-controlled movement of fructose through these pathways that causes it to contribute to greater triglyceride synthesis. The bottom line of this study is that fructose very quickly gets made into fat in the body.”

For the study, six people were given three different drinks. In one test, the breakfast drink was 100 percent glucose. In the second test, they drank half glucose and half fructose; and in the third, they drank 25 percent glucose and 75 percent fructose. The drinks were given at random, and neither the study subjects nor the evaluators were aware who was drinking what. The subjects ate a regular lunch about four hours later.

The researchers found that lipogenesis, the process by which sugars are turned into body fat, increased significantly when the study subjects drank the drinks with fructose. When fructose was given at breakfast, the body was more likely to store the fats eaten at lunch.

Dr. Parks noted that the study likely underestimates the fat-building effect of fructose because the study subjects were lean and healthy. In overweight people, the effect may be amplified.

----------------------------------------

So this doesn't mean you should stay away from fruit though, as fruit has nutrients and fiber.  But fruit juice will pack on the pounds.

Cinnamon may also significantly help people with type 2 diabetes improve their ability to respond to insulin, thus normalizing their blood sugar levels. Both test tube and animal studies have shown that compounds in cinnamon not only stimulate insulin receptors, but also inhibit an enzyme that inactivates them, thus significantly increasing cells' ability to use glucose.

So go ahead and sprinkle cinnamon on all your baking and treats, it is healthy and tasty, yay!

The Digestive System

The way I think of it is comparing the digestive system to a system of pipes. Over time, pipes can get clogged with all sorts of junk, preventing proper flow. So how do you get rid of clogged pipes? You introduce a substance that won't stay in the pipes, it will just move the clog through the system and free up the flow. That's exactly what fiber does for the digestive system. Just like a drain/pipe cleaner wouldn't stay in the pipes, fiber doesn't get digested and therefore does not enter our bloodstream.

The Gruesome Twosome

There are two types of fiber, soluble and insoluble fiber (the solubility refers to whether or not it is water soluble). Here's a fantastic article from Health Castle breaking down the different functions of both types of fiber. But to simplify each type of fiber's job

• Insoluble fiber works most like the pipe cleaner. It's gonna move all the waste through the system to make sure that you stay regular in your bowel movements as well as create a healthier digestive system
• Soluble fiber... here's a great quote from a cool blog called Wise Geek summing it up:

The short-chain fatty acids produced through the fermentation of soluble fiber in the large intestine serve to stabilize blood glucose levels, lower low-density lipoproteins (LDL) or "bad" cholesterol in the blood, increase the production of immune cells, and promote colon health."

What's a good amount consist of?

Well, it's a little different for everyone. But usually between 25-35 grams a day will do the trick. Here's a graph that shows exactly how much for men and women of different ages from The Harvard School of Public Health. Also, the Health Castle article mentions, "An average diet contains 75%:25% insoluble fiber: soluble fiber. When making a food choice decision, don't worry about choosing a specific type of fiber." Basically what they're saying is that a balanced diet consisting of the proper amount of servings of fruits and vegetables will get the necessary amount of both types.

Wondertwinpowersactivate!

Originally uploaded by CleverGirlBek

Ok. So I’m finally starting to catch up on this end….

I finally received my Dexcom Seven STS (Fedex in Fort Myers was holding it hostage and didn’t bother to notify anyone…Seems the shipper forgot to put our unit #) which, and this is the short version, tests my glucose and gives a result every 5 minutes….

The sensor that samples the interstitial fluid is really tiny, although the applicator scared the crap out of me… I’m not big on the “insertion” devices when it comes to my pump infusion sets (sub-q catheters) as I’m a bit of a control freak- I don’t like my subcutaneous needles to go fast- I can’t handle the anticipation and the build up- I like to put them in slow and mellow…. It hurts less that way, at least for me…

Anyway, I have been wearing this thing for 2 weeks and I’m so surprised that each sensor did stay on (with strategic adhesive reinforcements and glad press and seal during showers to protect the adhesive) for the two sessions and they were not uncomfortable (occasionally the one in my belly felt like it was giving me an electrical zap…annoying, but very intermittent….

I am realizing that there is a huge learning curve for these things… As there was with my pump, which I am relearning right now as well to help get in better control…

The transmitter is manageable – fairly small- like a small disposable lighter. This week I have been wearing it in my arm (way less painful than insulin injection or pump infusion set insertion in the arm…pleasantly surprised…) as having it in my belly last week showed a whole bunch of “noise”…More likely than not the noise was from my purpley lightning bolts of fury (stretch marks from my giant preggo belly when I was carrying the big guy)…So this week I tried the arm…

The receiver is another story- not crazy about it. It’s freaking huge. I rigged a hook to it to hang it from my waistband as it came close to taking a dive a few times, and it is not waterproof. I did order a great little pouch from diabetesmall.com but I’m kind of digging being able to check the screen without opening the velcro flap…Still undecided….
This week the receiver keeps losing contact with the sensor and transmitter and it is making me nuts- a simple thing like having the transmitter in contact with my mattress or the receiver near my laptop seems to disrupt it.… So far I know not to rely on any of the numbers but the dexcom is helpful for following trends and hopefully adjusting my insulin dosages/basal rates, but I’m still testing with finger sticks like a maniac (around 10 times a day lately) and noticing some fairly wide differences in numbers…

The one thing I am really disappointed about, that I may return this and try for the Navigator, is that this doesn’t alert you to potentially dangerous trends (potential lows and highs) but it does alert you when you go above or below a certain point. I knew this going in, but I don't think I realized how important that feature is in my world... As my hypoglycemia unawareness is pretty lousy and a low leaves me out of commission for up to 24 hours these days, and interstitial fluid readings are around 15-20 minutes behind finger sticks, I would like, at the very least, a higher “low” threshold… The other day I was registering as low at 90 but my fingerstick was 45. For me, that is too late and a little scary (especially in the middle of the night) and made me wonder if one of my reasons (I had a few) for wanting this bulky technology in my life is now invalid…

I mean, trends are going to save my life, but the way I look at it- the warning of lows, in advance, could save my kid’s life and my life and will give me back more time that I am losing from recovering from the highs and lows….

More on my Dexcom Seven experience over the next few weeks…. Still trying to figure it out and make a decision…

The difference between FRUIT sugar (fructose) and refined sugar (sucrose) is as
follows.

Fruit sugar is something known as FRUCTOSE
http://en.wikipedia.org/wiki/Fructose

"Fructose is broken down by the body slowly and is converted into SUCROSE and GLYCOGEN.
Fructose is often recommended for, and consumed by, people with diabetes mellitus
or hypoglycemia, because it has a very low Glycemic Index (GI 23) relative to cane
sugar."
http://en.wikipedia.org/wiki/Glycemic_Index

"Glycemic index (also glycaemic index, GI) is a ranking system for carbohydrates
based on their immediate effect on blood glucose levels. It compares carbohydrates
gram for gram in individual foods, providing a numerical, evidence-based index of
postprandial (post-meal) glycemia. The concept was invented by Dr. David J. Jenkins
and colleagues in 1981 at the University of Toronto."

Sucrose (common name: table sugar, also called saccharose) is a disaccharide (glucose
+ fructose) with the molecular formula C12H22O11.

This website explains it well http://waltonfeed.com/fructose.html

"There are differences between the different sugars. When we eat sucrose, our bodies
quickly break it down into roughly equal parts of glucose and fructose. Glucose
is the sugar our bodies use for both physical and mental energy. When our bodies
sense an increase of glucose in the blood, it immediately directs the pancreas to
push insulin into the blood stream. With the insulin, the body is able to burn the
glucose as energy. If there's too much glucose in the blood stream to be used as
energy, the glucose can be changed to glycogen, the body's short-term storage energy
supply. And if the glycogen pool is already full, the body will turn it into long
term storage in the form of fat.

Different blood-sugar effects possible after eating a high concentration of sucrose
sugar.

Different blood-sugar effects possible after eating a high concentration of sucrose
sugar.

Depending on the condition of the pancreas, the above graph shows what can happen
when a person eats a lot of sucrose sweets at one time. In each of the three cases,
the large amount of sugar dramatically raises the blood-sugar level but the results
can be radically different if no medication is given.

Eating a huge amount of sugar at once with it's resultant spike in the blood-sugar
level can cause stress to a weak pancreas as it struggles to deliver enough insulin
to bring down the blood-sugar to acceptable levels.

This cycle is especially hard on people who have an abnormal pancreas. If
the pancreas doesn't produce enough insulin that person is considered diabetic.
If it produces too much insulin they are considered hypoglycemic. These people will
generally suffer from an abnormal glucose level depending on what their condition
is. Checking the graph to the right, when a person eats too much sugar (sucrose),
there is a resulting rapid increase in their blood sugar level. If things are working
normally, the pancreas produces just enough insulin to bring the blood-sugar level
back down to normal. If they are diabetic and no medication is given, there isn't
enough insulin produced and the blood-sugar level remains elevated. In a hypoglycemic
person, as the blood-sugar level raises, their over-active pancreas dumps too much
insulin into the blood stream and they end up with low blood sugar levels which
creates it's own havoc.

Using fructose instead of sucrose puts a strong damper on many of these problems.
Your body can't use fructose without converting it into glucose in the liver. Actually,
most of the time, however, unless your body needs to immediately increase it's blood-sugar
level, the liver changes fructose into glycogen first. We have already mentioned
glycogen which is the body's short term energy supply. A typical adult will have
as much as 3/4 pound of glycogen in their various tissues at one time, mostly stored
in the liver and muscles. As the glucose level in the blood begins to drop, the
liver can rapidly convert this stored glycogen into glucose."

In short the reason why Fruit sugar is better for you than table sugar is that by
eating table sugar (Sucrose) our bodies go out of sync with our sugar levels as
the sugar is processed in the body extremely fast and in doing this the body informs
the pancreas to pump out insulin. Someone with a weak pancreas will have a hard
time doing this.

Fructose (Fruit sugar) is broken down more slowly which allows the body more time
to react to the sweetener that has been consumed. This puts less stress on the body
and also the pancreas which is good news for diabetics as they too can have sweet
tasting things but without the worry of a sudden sugar spike.

For more detail on this article, please visit:
Major Reference:
Google Answers

Well, after some handy dandy googling, I have an answer for the last one. When you eat a huge dinner or a large meal before bed, your stomach kicks into digestive mode and works all night to burn off that energy (glucose or something? dunno) so then when you wake up in the morning your stomach is empty and all sorts of digested out and needs some nom noms. Whereas if you ate a small dinner or nothing at all, when you go to bed your stomach is on off mode or fasting and remains that way soon after you wake up.

So, who knows, all of this could be complete bull but it's a good enough answer for me.

Rheumatoid arthritis (RA) is a common disease that affects about 1% of the population worldwide. Women are affected almost 3 times as often as men. The prevalence increases with advancing age, and 4% to 6% of the white population older than 65 years may have RA. Although the cause is unknown, evidence suggests an association between severe RA and HLA, particularly to alleles coding for a shared epitope on the HLA-DRB1 molecule.

Major features of active disease include symmetrical polyarthritis with joint swelling and tenderness and morning stiffness lasting for an hour or longer. Subcutaneous nodules, presence of rheumatoid factor (in about 80% of patients with RA), and radio graphically evident erosions or juxta-articular osteoporosis in or adjacent to the involved joints are further characteristics of RA.

The onset and clinical course of RA are variable. Gradual onset is most common. About 20% of patients will have a monocyclic course, which will abate within 2 years, whereas the rest will have a polycyclic or progressive course.¹ The long-term prognosis of patients with abrupt onset of disease is similar to that for patients with gradual onset of disease.²

Rheumatoid arthritis is one of the most common causes of disability. After 12 years of disease, more than 80% of patients with RA are partially disabled, and 16% are completely disabled.³ Life expectancy is shortened by an average of 7 years in men and 3 years in women, an outcome equivalent to the increased mortality of patients with Hodgkin disease, diabetes, and stroke.⁴ Factors contributing to the poor prognosis include the presence of extra-articular disease and infections, as well as complications of treatment such as gastrointestinal (GI) toxic effects of nonsteroidal anti-inflammatory drugs (NSAIDs).

MANAGEMENT PRINCIPLES

The goals of therapy for RA are to alleviate pain, control inflammation, preserve the ability of the patient to function in activities of daily living and work, and prevent joint destruction. Appropriate and timely therapeutic intervention after accurate diagnosis diminishes not only the symptoms but also the progress of RA. The primary care physician has a crucial role in this process by early recognition of the symptoms of RA, leading to its diagnosis and use of the resources necessary to establish a successful treatment program to achieve these goals, and by participating in the ongoing management of the patient with RA.Early in the course of RA, education on the disease and vocational, lifestyle, and family counseling must be provided. Patients are best served by a multidisciplinary team that includes a rheumatologist and other specially trained medical personnel, including nurses and occupational and physical therapists skilled and knowledgeable about RA. Physical modalities such as joint protection, orthotics and other adaptive devices, and exercises improve the symptoms, function, and well-being of the patient. Adequate rest reduces the fatigue associated with active RA, and resting the involved joints lessens the symptoms of inflammation.

THERAPY

Nonsteroidal anti-inflammatory drugs reduce inflammation and help relieve pain but seldom completely eliminate signs and symptoms of active arthritis. They inhibit 1 or both types of cyclooxygenase (COX). Cyclooxygenase-1 is constitutively expressed in the GI mucosa, kidneys, platelets, and vascular endothelium. Cyclooxygenase-2 is functionally expressed and promotes the elaboration of prostaglandins in inflamed tissues.

Selective blockage of COX-2 may lead to an improved safety profile for these agents. Celecoxib and rofecoxib are the first such agents available in the United States that selectively block COX-2. Rofecoxib is withdrawn from the market due proven increase in cardiac risk.  Of importance, the efficacy of these COX-2 inhibitors does not differ substantially from that of conventional NSAIDs. Their putative advantage is principally because of a reduced rate of adverse events, especially upper GI bleeding.⁵ Cyclooxygenase-2 inhibitors should be considered in patients at high risk of GI bleeding, including those older than 65 years and those with a previous history of GI bleeding. Despite advantages, these drugs may be associated with important adverse reactions, including allergy and fluid retention, and like other NSAIDs should be used with caution in patients with renal insufficiency.

Glucocorticoids are the most potent suppressors of inflammation and may be needed to control severe polyarticular disease until disease-modifying antirheumatic drugs (DMARDs) have been added and become effective. At that point, the glucocorticoids should be tapered and discontinued. Glucocorticoids should not be used alone in the management of RA. Oral prednisone or an equivalent is given in dosages typically ranging between 2 and 15 mg/d, often in divided doses (eg, 2 mg twice a day). A split-dosing regimen is frequently necessary because the anti-inflammatory effect is relatively short. It is preferable, but often not possible, to avoid long-term glucocorticoid therapy in patients with RA because of the well-appreciated adverse effects of these drugs. Systemic extra-articular manifestations such as rheumatoid vasculitis may require treatment with initial prednisone dosages of 40 to 60 mg/d, tapering according to response.⁶ Intra-articular injection of glucocorticoids is an effective means for reducing pain and inflammation in individual recalcitrant joints.

Disease-modifying antirheumatic drug therapy is associated with reduced morbidity and mortality in patients with RA.⁷ It should be used when the diagnosis of RA has been established and before erosive change appears. Disease-modifying antirheumatic drugs are usually given with NSAIDs and glucocorticoids, if needed. The DMARDs currently in use are listed in Table 1. The mechanism of action of most of these agents is diverse and to a variable extent overlapping. For many of the agents, the mechanism of action is defined incompletely, whereas for some, including the new class of tumor necrosis factor (TNF) blockers, it is better understood.

For patients with mild disease, hydroxychloroquine is often the first drug of choice because of ease of use and its favorable toxicity profile. Retinopathy due to hydroxychloroquine rarely develops when appropriate dosages are used. The onset of antirheumatic disease activity occurs in about 3 to 4 months in almost 50% of patients, although 6 months may be needed for the full benefit to be realized. For patients with moderately active or severe newly diagnosed disease, methotrexate or sometimes sulfasalazine is a preferred initial choice. In patients with continuing active established disease, methotrexate may be used in combination with other agents including hydroxychloroquine, sulfasalazine, or both or cyclosporine, azathioprine, and the more recently available DMARDs.⁹

For patients with acute and severe disease, a combination of DMARDs, prednisone, and an NSAID may be initiated; the dose of prednisone should be tapered during the ensuing weeks to months as disease control improves.

Because of its favorable efficacy and toxicity profile, methotrexate is regarded by many rheumatologists as the anchor therapy for RA. The initial dosage is usually 7.5 to 10.0 mg/wk, titrated upward to an average dosage of 12.5 to 15.0 mg/wk, although dosages of 20 to 30 mg/wk (if tolerated) may be necessary to realize this drug’s therapeutic potential before the response is deemed “inadequate.” Methotrexate may be given in tablet or liquid form; the liquid form is substantially less expensive than tablets, and injection may be associated with less stomatitis and GI upset. Appropriately managed, methotrexate can be used effectively for long periods to control RA. Although generally well tolerated, methotrexate can cause GI upset and hepatotoxicity including liver fibrosis and cirrhosis. Concomitant alcohol use is an important risk factor for methotrexate-related hepatotoxicity, and thus alcohol should not be used by patients taking this drug. Methotrexate can also cause a syndrome of pulmonary hypersensitivity manifested by dyspnea, cough, and fever and should not be used in patients with hepatic or renal insufficiency or severe lung disease. Supplemental folate (usually 1 mg/d) seems to reduce the occurrence of other adverse effects, including stomatitis, hair thinning, and bone marrow suppression. In patients taking methotrexate, physicians should avoid prescribing antifolate drugs such as sulfamethoxazole for sinusitis or cystitis, which may precipitate pancytopenia.

Use of DMARDs has substantially improved disease control and the long-term outlook for patients with RA. Their use may be associated with a lower incidence of extra-articular disease manifestations such as systemic vasculitis. In a series of more than 3000 patients monitored for up to 20 years, patients who had received DMARD therapy had a 30% reduction in long-term disability and improvement in survival compared with patients who had received NSAIDs alone.⁷ Despite these successes, major challenges exist. For example, DMARDs are becoming more accepted among practicing physicians and their patients¹⁰ however, adverse effects or failure of the drug to produce long-term disease control often leads to a change in DMARD treatment.

To improve disease control, therapies that contain combinations of DMARDs are often used. About 50% of patients with RA treated by rheumatologists are prescribed combination therapies with either 2 or 3 DMARDs. The combination of methotrexate, hydroxychloroquine, and sulfasalazine is among the most popular regimens. Methotrexate is often combined with other DMARDs including cyclosporine, but many other combinations of DMARDs have also been used.

In addition to hydroxychloroquine and methotrexate, other traditional DMARDs include penicillamine, gold, and sulfasalazine. Sulfasalazine was among the first drugs to be developed for the treatment of RA and may be chosen as the initial DMARD for patients with no allergy to sulfa, rather than hydroxychloroquine or methotrexate. The use of gold or penicillamine is seldom recommended because of the limited efficacy and the pronounced incidence of adverse effects associated with these drugs.

Three to 6 months may be needed before agents such as gold, hydroxychloroquine, and even sulfasalazine are effective. If the response is inadequate after 6 months of treatment, a second DMARD should be added or the DMARD regimen should be changed.

In the past year, 3 new DMARDs, etanercept, infliximab, and leflunomide, have been approved for the treatment of patients with RA.^11,12 Etanercept and infliximab are TNF-α antagonists that have powerful anti-inflammatory effects in patients with RA. Tumor necrosis factor is a potent inflammatory cytokine expressed in increased amounts in the serum and synovial fluid of patients with RA. It promotes the release of other proinflammatory cytokines, particularly interleukin (IL) 1, IL-6, and IL-8 and stimulates protease production. Etanercept consists of fusion monoclonal antibody composed of 2 identical chains of recombinant human TNF-α receptor fused with the Fc portion of human IgG1. In vitro it binds to soluble TNF. About 70% of patients receiving subcutaneous etanercept at dosages of 25 mg twice a week have substantial improvement in the extent of joint inflammation, often within 1 to 2 weeks after initiation of therapy. This improvement can be enhanced by combination with methotrexate. Adverse effects of etanercept are influenza-like symptoms and reactions at the injection site, which usually abate after the first few injections. The efficacy of infliximab, a recombinant TNF receptor fusion protein, seems to be roughly equivalent to that of etanercept. Infliximab is given intravenously once every 8 weeks, a regimen that may be more convenient for some patients. Potential long-term risks of these TNF-α antagonists have not been established. Infliximab may be associated with development of autoantibodies such as antinuclear antibodies. To date, neither drug has an increased risk of malignancy, autoimmune disease, or infection, issues that are the subject of ongoing postmarketing surveillance. The cost of these drugs is about $10,000 to $12,000 a year, generally higher for etanercept than infliximab. The available TNF-α antagonists should be considered in patients with recalcitrant disease not controlled by methotrexate.

Leflunomide is a pyrimidine synthesis inhibitor with clinical efficacy generally equivalent to methotrexate.¹³ Adverse effects reported include rash, alopecia, allergy, weight loss, thrombocytopenia, and diarrhea. Diarrhea often occurs early in the course of treatment and may abate, but discontinuation of the drug is necessary when the diarrhea cannot be ameliorated with dose reduction or concomitant use of antidiarrheal agents.

Serious extra-articular disease manifestations including vasculitis, scleritis, and recalcitrant serositis generally require systemic glucocorticoids and may necessitate the use of immunosuppressive agents such as cyclophosphamide. In my opinion, the only indication for cyclophosphamide in the treatment of RA is severe extra-articular disease, especially vasculitis.

Of importance, the decision about the use and aggressiveness of DMARD therapy should not be based solely on the presence or absence of the rheumatoid factor. Early in the course of RA, the rheumatoid factor may be absent, whereas in patients with established poly articular arthritis, absence of the rheumatoid factor is not invariably associated with mild disease and good disease outcome. Treatment must be tailored to the disease manifestations and needs of the individual patient. Consultation with a rheumatologist is helpful for patients who are pregnant or considering pregnancy because many antirheumatic drugs have severe fetal toxic effects including teratogenicity. Management suggestions for several clinical scenarios involving patients with RA are listed in Table 2.

When the symptoms of RA are well controlled, the glucocorticoids should be tapered, and the NSAIDs may also be tapered or used as needed. As a generalization, DMARD therapy should be continued indefinitely; however, if the patient does well and has no signs of active disease for at least 1 year, DMARD therapy could be carefully tapered. With combination DMARD therapy, one of the DMARDs could be tapered if the patient has been in remission for at least 6 months. Methotrexate can be considered as an “anchor” therapy and generally continue this drug for the longest period. Of note, less than 5% of patients with bona fide seropositive RA remain in long-term disease-free remission.

Rheumatoid arthritis is a serious disease. Follow-up early in the course of disease and in patients with poorly controlled disease should be every 2 to 6 weeks. Patients with well-controlled disease may be seen every 3 to 6 months. The primary care physician has an important role in the management of RA and can effectively guide and monitor routine therapy, with periodic consultation by a rheumatologist as needed. Assessment of disease activity and treatment efficacy is enhanced substantially with serial use of standard outcome measures, including duration of morning stiffness, severity of fatigue, presence and degree of joint pain and stiffness including joint counts, global and disease-specific health assessment instruments such as the modified Health Assessment Questionnaire, erythrocyte sedimentation rate, and radiographs of involved joints.

Appropriate medical care for patients with RA includes immunization and prompt treatment of infections. Patients with RA have a high risk of infections even if they are not taking DMARDs but particularly when they are taking immunosuppressive drugs. Several medications used to manage RA, including NSAIDs, cyclosporine, and glucocorticoids, may cause or exacerbate hypertension. Rheumatoid arthritis is associated with an increased incidence of pulmonary disease, and patients who smoke have an especially high rate of lung disease. In patients at high risk of GI bleeding, including elderly women and those with a previous history of GI bleeding, prophylaxis is achieved with agents such as proton pump inhibitors and misoprostol. As a general principle, use of NSAIDs should be avoided when possible and certainly discontinued when symptoms diminish. Virtually all patients with RA have or develop osteoporosis as a complication of the disease or its treatment. Adequate intake of calcium (1200-1500 mg/d) and vitamin D (400 IU/d) is important. In all patients receiving long-term corticosteroid therapy, including men, an antiresportive agent such as bisphosphonates or calcitonin should be considered. In postmenopausal women, estrogen replacement therapy or agents such as raloxifene may be considered. Finally, mouth and eye moisturization is necessary for patients with sicca complex symptoms.

Understanding the relationship of disease susceptibility and severity with genetic factors may provide an avenue for individualized treatment of patients with RA in the future. It may be possible to treat patients lacking genetic markers of severe disease with milder agents, while those with markers of severe disease may be treated more aggressively. More than 80 drugs are currently being developed for treatment of RA; thus, further advances in the management of the disease are forthcoming.

Questions About Treatment of RA

1. Which one of the following would be an acceptable therapeutic program for a patient with early mild RA?

1. Hydroxychloroquine with an NSAID
2. Hydroxychloroquine, methotrexate, and an NSAID
3. Methotrexate and prednisone at 5 to 15 mg/d
4. Etanercept and prednisone
5. Leflunomide and sulfasalazine

2. Which one of the following regimens would be appropriate for a patient with RA and new-onset systemic vasculitis?

1. Azathioprine, hydroxychloroquine, and prednisone at 10 to 15 mg/d
2. Prednisone, 20 mg/d, and methotrexate, 25 mg/wk
3. Prednisone, 40 to 60 mg/d, and cyclophosphamide
4. Cyclosporine and prednisone at 20 to 30 mg/d
5. Prednisone, 40 to 60 mg/d, and immunoabsorption column treatment

3. Which one of the following situations is not a relative contraindication to the use of etanercept?

1. Patient with history of tuberculosis exposure
2. Patient with history of lymphoma
3. Patient with active chronic infection
4. Patient with newly diagnosed RA
5. Patient with established RA receiving hydroxychloroquine and methotrexate

4. Which one of the following statements about the clinical course of RA is false?

1. The median life expectancy of patients with RA is the same as that for the general population
2. Most patients with RA have some disability after 12 years of disease
3. Predictors of poor outcome in patients with RA include the extent of radiographic erosions, female sex, and functional class
4. Patients in whom the rheumatoid factor is present have a worse prognosis than those with seronegative disease
5. Disease-free remission is unusual

5. Which one of the following statements about COX is true?

1. Cyclooxygenase-1 is constitutively expressed in the gastric mucosa, kidney, and platelets
2. Use of the currently available selective COX-2 inhibitors is safe in patients with renal failure
3. Currently available selective COX-2 inhibitors have been proved in multiple clinical trials to be safe in patients who are taking warfarin
4. Cyclooxygenase-1 is functionally expressed and promotes the elaboration of prostaglandins important in the inflammatory cascade
5. Selective COX-2 inhibitors are not associated with risk of GI bleeding Correct answers: 1. a, 2. c, 3. e, 4. a, 5. a

REFERENCES

1. Masi AT. Articular patterns in the early course of rheumatoid arthritis. Am J Med. 1983;75(suppl 6A):16-26.
2. Jacoby RK, Jayson MI, Cosh JA. Onset, early stages, and prognosis of rheumatoid arthritis. BMJ. 1973;2:96-100.
3. Sherrer YS, Bloch BA, Mitchell DM, Young DY, Fries JF. The development of disability in rheumatoid arthritis. Arthritis Rheum. 1986;29:494-500.
4. Mitchell DM, Spitz PW, Young DY, Bloch BA, McShane DJ, Fries JF. Survival, prognosis, and causes of death in rheumatoid arthritis. Arthritis Rheum. 1986;29:706-714.
5. Wolf MM, Lichtenstein DR, Singh G. Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 1999;340:1888-1899.
6. Matteson EL, Conn DL. Extraarticular manifestations of rheumatoid arthritis. In: Weisman MH, Weinblatt ME, eds. Treatment of the Rheumatic Diseases. Philadelphia, Pa: WB Saunders Co; 1995:52-67.
7. Fries JF, Williams CA, Morfeld D, Singh G, Sibley J. Reduction in long-term disability in patients with rheumatoid arthritis by disease-modifying antirheumatic drug-based treatment strategies. Arthritis Rheum. 1996;39:616-622.
8. American College of Rheumatology Ad Hoc Committee on Clinical Guidelines. Guidelines for monitoring drug therapy in rheumatoid arthritis. Arthritis Rheum. 1996;39:723-731.
9. Borigini MJ, Paulus HE. Rheumatoid arthritis. In: Weisman MH, Weinblatt ME, eds. Treatment of the Rheumatic Diseases. Philadelphia, Pa: WB Saunders Co; 1995:31-51.
10. Ward MM, Fries JF. Trends in antirheumatic medication used among patients with rheumatoid arthritis, 1981-1996. J Rheumatol. 1998;25:408-416.
11. Weinblatt ME, Kremer JM, Bankhurst AD, et al. A trial of etanercept, a recombinant tumor necrosis factor recepton:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. N Engl J Med. 1999;340:253-259.
12. Moreland LW, Baumgartner SW, Schiff MH, et al. Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75)-Fc fusion protein. N Engl J Med. 1997;337:141-147.
13. Mladenovic V, Domljan Z, Rozman D, et al. Safety and effectiveness of leflunomide in the treatment of patients with active rheumatoid arthritis. Arthritis Rheum. 1995;38:1595-1603.

A disease of middle-aged and older felines, Diabetes occurs more commonly in male cats. Risk factors include obesity, diet, genetics and damage to pancreas. Clinical manifestations are increased thirst, diet and urination, weight loss, skin and hair changes and liver and kidney disease. There is lethargy, weakness of hind legs and wobbly gait. Often these, alongside urination outside the litter box, are the first signs that the cat owner may notice of this insidious illness.

Once the diagnosis is reached through analysis of urinary and blood glucose levels, treatment is initiated. In the majority of cases it involves a regimen of insulin injections. In Type II disease, oral hypoglycemic agents are given at times. Though this is rare and it is often easier for owners to inject their cats than feed them pills. Even though there is no cure for Diabetes, prompt and appropriate treatment ensures that the diseased cats live a normal and healthy life.

Diabetic cats are usually advised a prescription diet. It is important to feed the cats this at regular times through the day alongside the insulin dosage. It is equally significant to ensure that the cats get regular exercise. For if any of the three elements - insulin dose, dietary intake and exercise - are out of sync with each other, the glucose balance of the animal may be altered. If all the three aspects are maintained under control though, the cat can be expected to live a long and happy life.

One of the most common gestational diabetes test is the oral glucose tolerance test. This is a quick test where pregnant women are required to drink a sweetened liquid which contain 50g of glucose. After 30-60 minute a blood sample will be taken for measurement. Result of this test will determine whether you should take a more complicated test which is called the 100-gram oral glucose tolerance test.

In stable diabetic patients, each percentage point of HbA_1c corresponded to about a 29 mg/dL increment in estimated average glucose.

Citation(s):

Nathan DM et al. Translating the A1C assay into estimated average glucose values. Diabetes Care 2008 Aug; 31:1473.

Currently, many major medical organizations advise tight glucose control for critically ill patients, and these recommendations have been adopted in many intensive care units around the world, according to background information in the review study by U.S. researchers.

They analyzed data from 8,432 patients in 29 previous studies and found no significant difference in hospital death rates for patients on tight glucose control (21.6 percent) and those receiving usual care (23.3 percent).

The researchers also found that tight glucose control was not associated with a significantly decreased risk for new need for dialysis (11.2 percent vs. 12.1 percent), but was associated with a significantly decreased risk (10.9 percent vs. 13.4 percent) of septicemia (generalized illness due to bacteria in the blood).

However, patients on tight glucose control had about a five-fold increased risk of hypoglycemia (13.7 percent vs. 2.5 percent).

"Given the overall findings of this meta-analysis, it seems appropriate that the guidelines recommending tight glucose control in all critically ill patients should be re-evaluated until the results of larger, more definitive clinical trials are available," concluded Dr. Renda Soylemez Wiener, of the Department of Veterans Affairs Medical Center in White River Junction, Vt., and Dartmouth Medical School, in Hanover, N.H., and colleagues.

The study was published in the Aug. 27 issue of the Journal of the American Medical Association.

But, Simon Finfer, of the George Institute for International Health, and Anthony Delaney, of the Royal North Shore Hospital in Sydney, Australia, wrote in an accompanying editorial that it's possible that some of the studies included in the meta-analysis were flawed or that the meta-analysis itself was flawed.

"Possible explanations for the discordant results of the study by van den Berghe et al and the meta-analysis by Wiener et al are that the meta-analysis is flawed, the studies that form the basis of the meta-analysis are flawed or inherently different, or the findings of the study by van den Berghe et al occurred due to random chance or as a result of another unique factor interacting with tight glycemic control."

They added that "those investigating tight glycemic control should take a step back and address the fundamental questions of defining quality standards for tight glycemic control, finding affordable methods of frequent and highly accurate measurement of blood glucose in the ICU, and conduct multicenter efficacy studies to determine if tighter glycemic control can reduce mortality under optimal conditions. If tighter glycemic control can be proven effective in optimal conditions, determining how to make that benefit available to millions of critically ill patients in both developed and resource-poor countries around the world would be a truly worthwhile challenge. There is no simple or clear answer to the complex problem of glycemic control in critically ill adults; at present, targeting tight glycemic control cannot be said to be either right or wrong."

More information

The American Thoracic Society has more about critical care.

— Robert Preidt

SOURCE: Journal of the American Medical Association, news release, Aug. 26, 2008

Last Updated: Aug. 26, 2008

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