Why Should you stretch?

For all of those who have worked out semi-hard at some point in their life, they will most likely understand the situation that follows the next day and even more pronounced two days later; dreaded sore muscles!  There has been a lot of research in this area as far as causes and alleviating factors.  How do we prevent or at least reduce the dreaded muscle soreness?!  First and foremost just about every article that I found says that pre-exercise stretching does not help prevent injury or muscle soreness.  The best thing to do before working out is just a low to mid-grade warm up of jogging and perhaps active stretching.  Yet, you must be careful with active stretching (dynamic stretching like high knees and the like).  It is very easy to do motions that can lead to injury with this if it is not given proper attention.  It seems the goal of warm-up is precisely that…warming up the muscles.  Static stretching did show some prevention, yet fairly iffy and low, of tendon/ligament injuries.

So, what can we do to help reduce that painful walk the day after we work out.  Well, this depends on the cause of that soreness.  If it is lactic acid(most common thought) then massage and stretching seems to be pretty effective for reducing (yet not preventing) post-workout pain.  Now, you have to do massage and stretching fairly soon after your workout.  The idea behind this is that by massage and stretching you will, in a sense, “squeeze” the lactic acid out of your muscles so as to help prevent acid buildup and muscle breakdown.  For, sore muscles really are just broken down muscles, in this case (this is a good reason to have a good source of protein after a workout so that your muscles can rebuild for they are made of protein).  Another cause of soreness is due to muscle spasms which are direct injury to the muscle.  Stretching these can help remove the “knot” but the best way to treat these it would seem is to ice/take NSAIDS (anti-inflammatories) to reduce the swelling in the area and then slight stretching a few days later.  Rest is fairly important as well.  This covers the two main causes of muscle soreness.  If there are further needs I can do more research.  Below you will find the article excerpts to help give sources for the information I have just given.  Enjoy and remember, I just report and I am not a doctor!

The Results/Sources

It seems that much of the literature (yet not all) which I am finding says that pre-performance stretching does not lead to a statistically significant decrease in performance related muscular injuries (strains, pulled muscles and soreness).  Yet, many of them do mention that pre-performance stretching and warming up does help reduce the occurrence of musculotendenous related injuries (ACL, MCL, ankle sprains and the like).  So, while it seems that from a scientific study standpoint that stretching and warming up does not truly reduce the occurrence of muscular injuries it does have some benefit towards tendon problems and I think therefore is justified.  Now you know why you are doing it.  And knowing is half the battle.  Here are many quotes from conclusions from many studies.

No Benefit for injury reduction:

AUTHORS’ CONCLUSIONS: The evidence derived from mainly laboratory-based studies of stretching indicate that muscle stretching does not reduce delayed-onset muscle soreness in young healthy adults.  (Herbert RD, de Noronha M.  “Stretching to prevent or reduce muscle soreness after exercise.”  Cochrane Database Syst Rev. 2007 Oct 17;(4):CD004577.  University of Sydney, School of Physiotherapy, PO Box 170, Lidcombe, NSW, Australia, 1825. R.Herbert@fhs.usyd.edu.au)

*******

A systematic review of the literature was undertaken to assess the efficacy of static stretching as part of the warm-up for the prevention of exercise-related injuries. Computer-aided literature search for articles post-1990 and pre-January 2008 related to static stretching and injury prevention using MEDLINE, SPORT Discus, PubMed, and ScienceDirect databases. All relevant randomised clinical trials (RCTs) and controlled clinical trials (CCTs) satisfying inclusion/exclusion criteria were evaluated by methodological assessment to score the studies using accredited criteria. Seven out of 364 studies met the inclusion/exclusion criteria. All four RCTs concluded that static stretching was ineffective in reducing the incidence of exercise-related injury, and only one of the three CCTs concluded that static stretching did reduce the incidence of exercise-related injury. Three out of the seven studies noted significant reductions in musculotendinous and ligament injuries following a static stretching protocol despite nonsignificant reductions in the all-injury risk. All RCTs scored over 50 points (maximum possible score = 100), whereas all CCTs scored under 45 points. There is moderate to strong evidence that routine application of static stretching does not reduce overall injury rates. There is preliminary evidence, however, that static stretching may reduce musculotendinous injuries.  (Small K, McNaughton L, Matthews M.  “A systematic review into the efficacy of static stretching as part of a warm-up for the prevention of exercise-related injury.”  Res Sports Med. 2008;16(3):213-31. Department of Sport, Health and Exercise Science, University of Hull, Hull, England.)

*******

OBJECTIVE: Effect of Stretching on Sport Injury Risk: a Review To assess the evidence for the effectiveness of stretching for the prevention of injuries in sports.

DATA SOURCES: MEDLINE (1966 to September, 2002), Current Contents, Biomedical Collection, Dissertation Abstracts, the Cochrane Library, and SPORTDiscus were searched for articles in all languages using terms including stretching, flexibility, injury, epidemiology, and injury prevention. Reference lists were searched and experts contacted for further relevant studies.

STUDY SELECTION: Criteria for inclusion were randomized trials or cohort studies of interventions that included stretching compared with other interventions, with participants who were engaged in sporting or fitness activities. One author identified 361 articles reporting on flexibility, methods and effects of stretching, risk factors for injury, and injury prevention, of which 6 articles fulfilled the inclusion criteria for meta-analysis.

DATA EXTRACTION: Three independent reviewers blinded to the authors and institutions of the investigations assessed the methodologic quality of the studies (100-point scale) and reached consensus on disagreements. Details of study participants, interventions, and outcomes were extracted. Weighted pooled odds ratios were calculated for effects of interventions on an intention-to-treat basis.

MAIN RESULTS: Reduction in total injuries (shin splints, tibial stress reaction, sprains/strains, and lower-extremity and -limb injuries) with either stretching of specific leg-muscle groups or multiple muscle groups was not found in 5 controlled studies (odds ratio [OR] 0.93; 95% CI, 0.78 to 1.11). Reduction in injuries was not significantly greater for stretching of specific muscles (OR, 0.80; CI, 0.54-1.14) or multiple muscle groups (OR, 0.96; CI, 0.71-1.28). Combining the 3 ratings of methodologic quality, median scores were 29 to 60/100. After adjustment for confounders, low quality studies did not show a greater reduction in injuries with stretching (OR, 0.88; CI, 0.67-1.15) compared with high quality studies (OR, 0.97; CI, 0.77-1.22). Stretching to improve flexibility, adverse effects of stretching, and effects of warm up were not assessed by appropriate intervention studies.

CONCLUSION: Limited evidence showed stretching had no effect in reducing injuries.  (Hart L. “Effect of stretching on sport injury risk: a review.” Clin J Sport Med. 2005 Mar;15(2):113. McMaster University, Hamilton, Ontario, Canada)

********

In addition, the in vitro improvement in contraction strength resulting from prestretching44–47 has not been consistently observed in the world of athletics. It has been shown repeatedly that passive stretching can result in an acute loss of strength.48–53 Along the same lines, a recent study of elite female soccer players demonstrated that static stretching before sprinting resulted in worsened performance.54 Stretching too vigorously before an athletic event is likely to impair performance. The injury prevention role of stretching has to be balanced against this consideration on an individual athlete-to-athlete basis.  (Jeffrey Jenkins, James Beazell. “Flexibility for Runners”.  Clinics in Sports Medicine Vol 29 Issue 3 (July 2010))

In Favor:

Stretching and Stretching program.

Massage effects on Soreness

http://fitnesshealthtoday.com/the-5-major-benefits-of-stretching-after-exercise/

http://sportsmedicine.about.com/cs/flexibility/a/aa022102a.htm

http://www.mayoclinic.com/health/stretching/HQ01447

What is in Diet Coke and Diet Pepsi?

(ingredient lists come from the respective company websites, regular pop for each company just takes out aspartame)

Each ingredient in red has some kind of affect on your health that is most likely detrimental.  How detrimental, we shall see…

High Fructose Corn Syrup

Surprisingly enough Diet Pepsi does not have HFCS (High fructose corn syrup) in it.  HFCS is a sweetener used in many many foods in present day USA.  There has been a lot of media attention given to this sweetener which came on the food additive scene in the 1970s.  HFCS is a fructose-glucose sweetener which differs from sucrose (which is also fructose-glucose) in that, as it’s name implies, contains a higher ratio of fructose to glucose.  This gives a “sweeter” taste to the sugar, or carbohydrate.  There are different formulas of HFCS which have different ratios of Fructose to sucrose and therefore taste sweeter.

Metabolism of Fructose

So the reason why fructose gets such a bad rap is that metabolically it does some shady things, so to speak.

What fructose does is that it skips a major regulatory step in the carbohydrate metabolism cycle known as Glycolysis.  This step is catalyzed by phosphofructokinase, which you can see in the graph below (left side in the middle).  Fructose enters the graph on the right side 1/4 of the way down and the arrow which you want to follow goes down.  The dotted arrow to “fructose-6-phosphate” is a low affinity pathway where some fructose is turned into glucose and enters glycolysis under normal regulation.  What this means is that fructose, much more rapidly and freely, is turned into pyruvate which is then shuttled into Fatty acid synthesis since you are usually eating fructose under “fed” states and not “starving” states.  Fructose also decreases leptin and insulin levels.  Low insulin levels combined with high glucose levels in the blood (from eating/drinking a soda) leads to even more glucose being released into your blood stream.  This occurs because when insulin levels are low; glucose uptake by muscles and fat tissue decreases.  Now, the level of fructose that you would receive with one pop will not drastically lower your insulin levels but it does throw off the normal homeostatic system your body has set up to deal with a large influx of glucose.  So, when there is a lot of fructose and some glucose, then insulin will increase but not quite to the level that it should and there will be more glucose flowing through your arteries.  This excess glucose (while on the short term will not do too much) is what causes many of the problems in diabetics with uncontrolled blood sugar.  I can cover why this occurs in a subsequent “Health Update”

Fructose undergoes more rapid glycolysis in the liver than does glucose, because it bypasses the regulatory step catalyzed by phosphofructokinase (Figure 21–5). This allows fructose to flood the pathways in the liver, leading to enhanced fatty acid synthesis, increased esterification of fatty acids, and increased VLDL secretion, which may raise serum triacylglycerols and ultimately raise LDL cholesterol concentrations. A specific kinase, fructokinase, in liver, kidney, and intestine, catalyzes the phosphorylation of fructose to fructose 1-phosphate. This enzyme does not act on glucose, and, unlike glucokinase, its activity is not affected by fasting or by insulin, which may explain why fructose is cleared from the blood of diabetic patients at a normal rate. Fructose 1-phosphate is cleaved to D-glyceraldehyde and dihydroxyacetone phosphate by aldolase B, an enzyme found in the liver, which also functions in glycolysis in the liver by cleaving fructose 1,6-bisphosphate. D-Glyceraldehyde enters glycolysis via phosphorylation to glyceraldehyde 3-phosphate catalyzed by triokinase. The two triose phosphates, dihydroxyacetone phosphate and glyceraldehyde 3-phosphate, may either be degraded by glycolysis or may be substrates for aldolase and hence gluconeogenesis, which is the fate of much of the fructose metabolized in the liver.

Here is another quote from Harper’s Illustrated Biochemistry, 28e Chapter 18 :

Fructose enters glycolysis by phosphorylation to fructose 1-phosphate, and bypasses the main regulatory steps, so resulting in formation of more pyruvate (and acetyl-CoA) than is required for ATP formation.  In the liver and adipose tissue, this leads to increased lipogenesis, and a high intake of fructose may be a factor in the development of obesity.

Phosphoric Acid

Phosphoric acid is a major player in many homeostatic events in your body.  It plays a major role in acid/base equilibrium in your blood (and therefore your body), as well as calcium uptake/release via parathyroid hormone.  Seeing how important this mineral (phosphate) and its acid is to homeostatic pathways in the body we should think about adding it to our bodies willy-nilly, so to speak.  What happens when you have an increased load of phosphoric acid in your stomach and eventually in your blood serum is that the free calcium is bound by the Phosphate into Calcium Phosphate.  This takes calcium out of the bloodstream which is registered in the parathyroid which will then release parathyroid hormone.  When PTH is released the body recognizes, in a sense, that it needs more Calcium.  The major calcium store in the body is the bones.  So, when PTH is released it leads to a greater resorption of bone (loss of bone mass).  Now, after one pop this won’t lead to fragile bones, but over years and years of upregulated PTH release due to an inordinate amount of Phosphoric acid entering into the body, along with the very real occasion of the general public not getting enough dietary Calcium as it is, we can find ourselves with weaker and weaker bones.  (Ganong’s Review of Medical Physiology > Chapter 23, Endocrine Physiology, 3e > Chapter 5).

Aspartame

Aspartame consists of two amino acids, phenylalanine and aspartate, linked to a methanol backbone. Unlike the other artificial sweeteners that are usually excreted unchanged, aspartame can be metabolized. Therefore, it is not strictly non-caloric (4 Kcal/g) and forbidden in people with phenylketonuria. Aspartame is about 200 times sweeter than sucrose. Due to the small amount ingested at a time, its caloric contribution is negligible. The FDA approved aspartame first for use in dry foods in 1981, then as a general sweetener in 1996. Monsanto bought Searle and converted it into NutraSweet in 1984. The patent on aspartame expired in 1992.

ASIDE:  The last decade saw an explosive increase in the number of food products containing non-caloric artificial sweeteners. More than 6,000 new products were launched in the United States between 1999 and 2004. Currently, an ingredient search on foodfacts.com yields 3,648 products containing one or more of the five FDA approved artificial sweeteners. Sucralose is the most popular (1,500 products), followed by acesulfame potassium (1,103 products) and aspartame (974 products). Artificial sweeteners are most commonly used in carbonated drinks. They also are found in a variety of other products, from baby food (e.g., Pedialyte) to frozen food (e.g., Lean Pockets). With such a diverse selection, it is more likely that people will encounter artificially sweetened items when making the day-to-day choices on food and beverages. The National Household Nutritional Survey estimated that as of 2004, 15 percent of the population regularly were using artificial sweetener. IRI Consumer Report stated that 65 percent of American households bought at least one sucralose-containing product in 2008. Therefore, the total number of artificial sweetener consumers, either regular or sporadic, is probably much greater.

Surprisingly, epidemiologic data suggest the contrary (that artificial sweeteners are “health food”). Several large scale prospective cohort studies found positive correlation between artificial sweetener use and weight gain. The San Antonio Heart Study examined 3,682 adults over a seven- to eight-year period in the 1980s. When matched for initial body mass index (BMI), gender, ethnicity, and diet, drinkers of artificially sweetened beverages consistently had higher BMIs at the follow-up, with dose dependence on the amount of consumption. Average BMI gain was +1.01 kg/m² for control and 1.78 kg/m² for people in the third quartile for artificially sweetened beverage consumption. The American Cancer Society study conducted in early 1980s included 78,694 women who were highly homogenous with regard to age, ethnicity, socioeconomic status, and lack of preexisting conditions. At one-year follow-up, 2.7 percent to 7.1 percent more regular artificial sweetener users gained weight compared to non-users matched by initial weight. The difference in the amount gained between the two groups was less than two pounds, albeit statistically significant. Saccharin use was also associated with eight-year weight gain in 31,940 women from the Nurses’ Health Study conducted in the 1970s . (“Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings”. Yale J Biol Med. 2010 June; 83(2): 101–108.  Published online 2010 June.)  (This source links out to many articles for each topic covers…I would highly recommend taking a gander at this article.  Below is from this article as well.)

In addition, consensus from interventional studies suggests that artificial sweeteners do not help reduce weight when used alone. BMI did not decrease after 25 weeks of substituting diet beverages for sugar-sweetened beverages in 103 adolescents in a randomized controlled trial, except among the heaviest participants. A double blind study subjected 55 overweight youth to 13 weeks of a 1,000 Kcal diet accompanied by daily capsules of aspartame or lactose placebo. Both groups lost weight, and the difference was not significant. Weight loss was attributed to caloric restriction. Similar results were reported for a 12-week, 1,500 Kcal program using either regular or diet soda. Interestingly, when sugar was covertly switched to aspartame in a metabolic ward, a 25 percent immediate reduction in energy intake was achieved. Conversely, knowingly ingesting aspartame was associated with increased overall energy intake, suggesting overcompensation for the expected caloric reduction. Vigilant monitoring, caloric restriction, and exercise were likely involved in the weight loss seen in multidisciplinary programs that included artificial sweeteners.

On the flip side if one were to look at Coca-Cola’s website where they discuss the topic of Aspartame they come up with different information (Link).  I have yet to check all of the sources that are used for this article…but for HFCS they cite Corn Refiners Association who I would say are slightly biased seeing as they are looking for preserving profit and sales.  (HFCS is a corn based product).  Also, they cite mostly their own BIHW (Beverage Institute of Health and Wellness) for just about everything.  They do have some credible sources but perhaps I will have to cover these in a subsequent update.

Citric Acid

A quick aside for those who know of a certain person’s run in with some means stones:

Several sodas contained an amount of citrate equal to or greater than that of alkali and total alkali as a lemonade beverage commonly used to treat hypocitraturic calcium nephrolithiasis (6.30 mEq/l citrate as alkali and 6.30 as total alkali). These sodas were Diet Sunkist Orange, Diet 7Up, Sprite Zero, Diet Canada Dry Ginger Ale, Sierra Mist Free, Diet Orange Crush, Fresca and Diet Mountain Dew. Colas, including Caffeine Free Diet Coke, Coke Zero, Caffeine Free Diet Pepsi and Diet Coke with Lime, had the lowest total alkali (less than 1.0 mEq/l). There was no significant correlation between beverage pH and total alkali content.

CONCLUSIONS: Several commonly consumed diet sodas contain moderate amounts of citrate as alkali and total alkali. This information is helpful for dietary recommendations in patients with calcium nephrolithiasis, specifically those with hypocitraturia. It may also be useful in patients with low urine pH and uric acid stones. Beverage malate content is also important since malate ingestion increases the total alkali delivered, which in turn augments citraturia and increases urine pH.

So Citric acid is good for those who suffer from two certain causes of renal stones and this is about the only good use for dietary citric acid…generally, if you can avoid it you might as well.  Really I could not find anything horrible about this in the literature.  The only thing that I did find (though I could only get access to abstracts) was the relation between citric acid/phosphoric acid found in soft drinks and tooth enamel erosion.  It seems that The Dental Association and other dental agencies are advocating for restructuring the ingredients of soft drinks so as to help prevent the current problems faced with child and adult consumption of pop and poor oral hygiene.

This is all I have for now.  Truly the best thing to drink for a quick energy boost is some fruit drink or, if you are not lactose intolerant, some milk.  I didn’t cover all the aspects of pop which could be particularly harmful, but only the ones I felt were most important at this time.  If you would like me to cover more aspects please let me know by commenting.  I hope you enjoyed the read.

Yesterday, a group of pro-life Senators led by Senate Republican Leader Mitch McConnell (R-KY) and Senator John McCain (R-AZ) banded together, leading an effort to block a Senate Defense-spending bill that would have opened the door for taxpayer-funded abortions on military bases. The 56-43 vote in the U.S. Senate fell four votes short of the 60 votes the bill’s proponents needed to move it forward.

Dr. Charmaine Yoest, President and CEO of AUL Action, recognized McCain and his colleagues for outstanding work as they “led the fight to win today’s key vote rejecting taxpayer-funded abortion in the military.” The vote was a major setback for the abortion industry’s agenda in Washington as its leaders fight to expand abortion without limitations and at any price.

“The momentum is on the side of Life,” said Yoest. “We stopped taxpayer-funded abortion on military bases against overwhelming odds in the Senate. If one vote had gone the other way, the result would be different. That’s why we must remain steadfast in our fight.”

We’ve been updating you for weeks on our fight to stop the Burris Amendment to the Defense Authorization Bill, and – after yesterday – experts believe that this issue is now dead during this Congressional session.

“Our goal,” Yoest told Bench Briefs, “is to stop bad measures like the Burris Amendment. But we have a bigger goal too, which is to restore a culture of Life in America. If we are going to succeed, we’ll need a different Senate next year – a Senate that respects Life.”

National Review and The Washington Times both featured opinion pieces on the Burris Amendment by AUL’s Denise Burke this week, click here to read them.
On The Docket

Assisted Suicide Decision in Montana Underscores Need for Legislation

Engage, a quarterly legal journal from The Federalist Society, is featuring an article from William Saunders, AUL’s Senior Vice President of Legal Affairs. In the article, Saunders provides detailed legal analysis of Baxter v. Montana, a recent case in which a court determined that there is nothing in state law to prohibit assisted suicide.

“This is a murky issue right now,” says Saunders. “It’s unclear legally speaking what the answer is. Because common sense does not always prevail in the courts, a legislative solution is the only way to definitively ensure this practice is banned.”

The Montana ruling, which is out of line with other state and federal court decisions, begs a simple question: If the state won’t prevent assisted suicide, will the state allow the practice? AUL has a specific solution. Our model bill, the Assisted Suicide Ban Act, would completely ban the practice and clear up any “gray areas” created by the courts.

Read Saunder’s Engage piece on Baxter v. Montana by clicking here.

False “Promises” of Embryo-Destructive Research Touted at Senate Hearing

Last Thursday, the Senate Appropriations Subcommittee on Labor, Health and Human Services held a hearing on “The Promise of Human Embryonic Stem Cell Research.”  However, while many in the scientific community promote embryo-destructive research as full of “promise” and “hope,” the reality is that this research destroys lives.

“The American people do not want their tax dollars supporting research or experimentation on living human beings,” said Kellie Fiedorek, a member of AUL’s legal team who attended the hearing. “We are working to ensure that Congress does not allow research that destroys life, especially when non-destructive techniques have proven successful.”

The Senate is considering legislation, introduced by Senator Arlen Specter (D-PA), that would allow federal funding of embryo-destructive research.

Read more about this hearing by clicking here.

Votes could occur at any time. Please click on the link below to send a message to House and Senate Members! Act now!

What has happened up to this point in the health care reform debate? The U.S. House of Representatives and the U.S. Senate have passed different bills. On the question of preventing abortion funding, the House language is good, the Senate language is unacceptable. Outside the abortion context, neither bill has adequate conscience protection for health care providers, plans or employers.

What’s next? The two chambers need to agree on a final bill. It is not clear how this will be achieved. There is discussion of using a reconciliation bill, a budget measure that in the Senate cannot be filibustered and needs only 51 votes to pass.

Analyses of the House and Senate-passed bills can be found on our website at: www.nchla.org/issues.asp?ID=51.

Click the link below to log in and send your message:
http://actions.nchla.org/link/target/nchla/cJz7yz5B.aspx

Make no mistake about it: President Obama, Senator Reid, and Speaker Pelosi are pushing ahead with their government takeover of health care – this time, with a “new and improved” health care bill!

However President Obama’s new health care proposal still contains the greatest expansion of abortion since Roe v. Wade — and your tax dollars will still be paying for it.

We need your help right now, as the pro-abortion lobby has tightened its stranglehold on Congress and the White House. According to official White House visitor logs, President Obama has allowed Planned Parenthood unfettered access to his Administration. Planned Parenthood President, Cecile Richards, has privately met with President Obama’s staff to discuss health care reform on several occasions (with her first visit coming only days after his inauguration!). This open door policy demonstrates the imminent danger of taxpayer-funded abortions – unless we take immediate action.

Speaker Pelosi, Senator Reid, and President Obama are determined to reward their friends at Planned Parenthood with your tax dollars. In Pelosi’s own words, she will do anything and everything to pass health care reform: “If the gate is closed we will go over the fence. If the fence is too high, we will pole vault in. If that doesn’t work, we will parachute in. But we are going to get health care reform passed.”

Essential Diagnosis (symptoms)

• Flank Pain which can radiate into the groin area, Hematuria (blood in the urine)
• Nausea/Vomiting
• Frequency in urination, dysuria
• abdominal pain, rectal pain

Prevalence

male 2 times more common, middle-aged white men

Types of Stones

• 80%-95% calcium, 80% calcium oxalate, number 2 uric acid stones
• composition in decreasing frequency – calcium oxalate and CaPO4, calcium oxalate, struvite (MgAlPO4), CaPO4, uric acid, cystine

Stone disease is common, with the lifetime risk of stone formation in the United States exceeding 12% in males and 6% in females. Prevalence of stone disease varies by racial background and geographic location within the United States, with older white males and southeastern states having the highest prevalence. Seventy-five percent of most stones are composed of calcium salts (oxalate, phosphate), while uric acid and struvite stones (magnesium-ammonium phosphate stones that form secondary to urea-splitting organisms) constitute 10% each. Formation of calcium stones can be due to one or multiple factors that include hypercalciuria, hypocitraturia, hyperoxaluria, and hyperuricosuria. In patients with hyperparathyroidism or those who ingest large amounts of calcium or vitamin D or in patients who are dehydrated or immobilized, hypercalciuria promotes stone formation. (Current Medical Dx and Tx Chapter 38)

caffeine increased urinary calcium, magnesium and sodium (but not oxalate) in both stone formers and controls, and increased urinary citrate levels in stone formers (DynaMed Nephrolithiasis)

How they form.

The main cause is hypercalcinurea or a larger than normal amount of calcium in the urine.  This can be caused by excess calcium consumption or metabolism/absorption disorders.  Here is a quote from Current Medical Diagnosis and Treatment Chapter 23 Urologic Disorders:

Diet and fluid intake may be important factors in the development of urinary stones. Those afflicted with recurrent urinary stone disease are encouraged to maintain a diet restricted in sodium and protein intake. Sodium should be restricted to 100 mEq/d. Increased sodium intake will increase sodium and calcium excretion, increase monosodium urate saturation (that can act as a nidus for stone growth), increase the relative saturation of calcium phosphate, and decrease urinary citrate excretion. All of these factors encourage stone growth. Protein intake should be limited to 1 g/kg/d. An increased protein load can also increase calcium, oxalate, and uric acid excretion and decrease urinary citrate excretion. Carbohydrates and fats have not been proved to have any impact on urinary stone disease. Bran can significantly decrease urinary calcium by increasing bowel transit time and mechanically binding to calcium. Excess intake of oxalate and purines can increase the incidence of stones in predisposed individuals. Although a reduction in dietary calcium results in reduced urinary calcium, the concurrent increase in urinary oxalate may promote stone formation. Only type II absorptive hypercalciuric patients (see below) benefit from a low-calcium diet. Persons in sedentary occupations have a higher incidence of stones than manual laborers.

So you do not have to stop drinking milk right now unless you are known to have type II absorptive hypercalciuria.

Here is a quote from Smith’s General Urology about Oxalate

Oxalate is a normal waste product of metabolism and is relatively insoluble. Normally, approximately 10–15% of oxalate found in the urine originates from the diet; the vast majority is a metabolic by-product. Most of the oxalate that enters the large bowel is consumed by bacterial decomposition. Diet, however, can have an impact on the amount of oxalate found in the urine. Once absorbed from the small bowel, oxalate is not metabolized and is excreted almost exclusively by the proximal tubule. The presence of calcium within the bowel lumen is an important factor influencing the amount of oxalate that is absorbed. The control of oxalate in the urine plays a pivotal role in the formation of calcium oxalate calculi. Normal excretion ranges from 20 to 45 mg/day and does not change significantly with age. Excretion is higher during the day when one eats. Small changes in oxalate levels in the urine can have a dramatic impact on the supersaturation of calcium oxalate. The principal precursors of oxalate are glycine and ascorbic acid; however, the impact of ingested vitamin C (<2 g/day) is negligible.

Hyperoxaluria may develop in patients with bowel disorders, particularly inflammatory bowel disease, small-bowel resection, and bowel bypass. Renal calculi develop in 5–10% of patients with these conditions. Chronic diarrhea with fatty stools results in a saponification process. Intraluminal calcium binds to the fat, thereby becoming unavailable to bind to oxalate. The unbound oxalate is readily absorbed.

Excessive oxalate may occur secondary to the accidental or deliberate ingestion of ethylene glycol (partial oxidation to oxalate). This may result in diffuse and massive deposition of calcium oxalate crystals and may occasionally lead to renal failure.

How to prevent.

From Smith’s General Urology again:

Inhibitors of urinary stone formation other than citrate, magnesium, and sulfates have been identified. These consist predominantly of urinary proteins and other macromolecules such as glycosaminoglycans, pyrophosphates, and uropontin. Although citrate appears to be the most active inhibitory component in urine, these substances demonstrate a substantial role in preventing urine crystal formation. The N–terminal amino acid sequence and the acidic amino acid content of these protein inhibitors, especially their high aspartic acid content, appear to play pivotal inhibitory roles.  Fluoride may be an inhibitor of urinary stone formation.

As you can see citrate is among those chemicals that helps to prevent stones.  For those who perhaps enjoy Sundrop or Mountain Dew or other sodas made with citric fruit juices this is good news.  These contain citric acid or citrate.  This does not mean they are good for you, but it is one plus among many many negatives.  Sundrop.  Some of the many negatives are caffeine (see above), dehydration, and more acidic urine (higher risk of uric acid stones).

As always, I hope this helps each of you be more informed.  I just report.  If you have any questions please feel free to post.

Your tax dollars are about to create abortion “mega-marts” across the nation. In fact, it’s already begun.

Planned Parenthood – the world’s largest abortion provider – has obtained a 78,000 square foot building in Houston, Texas that they are converting into a gargantuan abortion clinic. This new abortion mill will be the largest such facility in the United States with an entire wing dedicated solely to late-term abortions – and your tax dollars will be paying for it!

Is this what you want your tax dollars spent on?

Under the guise of “health care” reform, the Senate recently authorized the largest expansion of taxpayer-funding for Planned Parenthood in decades. This “health care” bill actually routes taxpayer dollars to Planned Parenthood as an “essential community provider”! In addition, it subsidizes insurance plans that cover elective abortions with your tax dollars, imposes a mandatory abortion tax on pro-life Americans who happen to be enrolled in such plans, and could potentially require all health care plans to cover abortions as “preventive care.”

How many abortion mega-marts will the Senate health care bill fund in the coming months if it becomes law?

I want to update you this morning on the health care battle here in Washington, D.C.

The debate on Capitol Hill is reaching a boiling point.  The Democratic leadership in Congress has elected to bypass the accepted conference process – where both Houses of Congress work together to craft a final bill – and are instead working out a secret deal behind closed doors.

Many of us don’t like what politicians do when we can see them, let alone what happens when we can’t.

While the House-passed bill includes the Stupak-Pitts amendment (which prohibits taxpayer funding of abortions), the Senate-passed bill subsidizes insurance plans that cover abortions and, for the first time in history, could allow the federal government to require private insurance plans to cover abortions.  With the pro-abortion Democratic leadership calling the shots, the final bill is bound to mirror the Senate’s version.

Thomas Jefferson once said, “To compel a man to furnish contributions of money for the propagation of opinions which he disbelieves and abhors, is sinful and tyrannical.”

And this is exactly what is at stake here, along with thousands (and perhaps millions) of babies’ lives which currently hang in the balance.

Americans United for Life’s legal team is working tirelessly to ensure that every member of Congress understands the deviously-written abortion language in the Senate bill and knows that this language is contrary to what the vast majority of Americans want.

A recent national Quinnipiac University poll found that 72% of voters don’t want public funding for abortion in the bill, and yet Congress continues to ignore the will of the American people.

Last week, AUL Staff Counsel Mary Harned briefed Capitol Hill staff members on the problems with the Senate bill.  She presented some must-see charts on Abortion in Health Care which you can see by clicking here and here.

I know that there is much more to be done.

I also know that this fight is far from over, and if we all continue to put pressure on Washington, we will win this battle for life.

And, on that note, I want to remind you that we have a major opportunity coming up next week. The national March for Life in Washington, D.C. takes place on January 22^nd, and we would love to hear from you if you are planning on attending.

Finally, we are working on an exciting new project that will give you the opportunity to participate in the March for Life, even if you cannot make it to D.C., so stay tuned for more information over the next few days.

As always, thank you for your generous and faithful support, which helps us to defend life here in Washington, D.C., across the United States, and around the world.

We desperately need your help as the U.S. Senate moves on pro-abortion health care legislation, so please join us for a Stop the Abortion Mandate Coalition live audiocast roundtable tomorrow night – Tuesday, December 15^th at 9 p.m. ET – to find out what you can do to take action on this urgent issue.

LIVE AUDIOCAST DETAILS:

WHAT: Stop the Abortion Mandate Urgent Audiocast

DATE: Tuesday, December 15th

TIME: 9 PM Eastern, 8 PM Central, 7 PM Mountain, 6 PM Pacific

Register now at: www.StopTheAbortionMandate.com/audiocast

Expert presenters include:

• CHARMAINE YOEST, Americans United for Life
• MARJORIE DANNENFELSER, Susan B. Anthony List
• TONY PERKINS, Family Research Council
• KRISTAN HAWKINS, Students for Life of America
• DOUGLAS JOHNSON, National Right to Life Committee
• KRISTEN DAY, Democrats for Life
• WENDY WRIGHT, Concerned Women for America
• DAVID BEREIT, 40 Days for Life

JOIN US TO HEAR…

• The LATEST UPDATES on abortion and its inclusion in the Senate health care legislation…
• What’s at stake if the abortion industry successfully pushes their agenda through passage of this pro-abortion bill…
• What you can do SPECIFICALLY to help us BLOCK this NOW.

We hope you can join us.  Thank you for helping defend life!

I have sent a letter to Planned Parenthood challenging them to tell you and every American taxpayer just how much they stand to gain from the health care bill and federal funding for abortion.

Planned Parenthood is the world’s largest abortion provider, with an annual budget in excess of $1 billion – that’s right, $1 billion – and posted an $85 million profit last year. Planned Parenthood also received $350 million in federal funding in 2007.

The number of federal government “bailouts” of private businesses over the past year is bad enough – but forcing American citizens to finance the abortion industry under the guise of “health care” cannot be accepted. The taking of human life is not health care. That’s why Americans United for Life is fighting back against abortion lobbyists in the U.S. Senate. Will you join our fight today?

Every year, well over 1,000,000 children lose their lives through abortion in America. For decades, existing federal law has prohibited the use of taxpayer funds from paying for abortions. But now a radical change would take place if the Democrat’s health care bill becomes law, our government would force pro-life taxpayers to pay for abortions.

Senate Democrats are perilously close to passing a health care bill that does not include language prohibiting federal funding of abortion; in fact, it explicitly includes federal funding for abortions and for insurance plans that include abortion coverage. If this version of the bill passes, there’s virtually no way the final version will protect life when it is signed into law by President Obama.

We worked with pro-life Senators to have a mirror version of the Stupak-Pitts Amendment included in the Senate bill. But pro-abortion Senators like Barbara Boxer, Claire McCaskill, and others who have publicly stated the bill will not pass with any pro-life language prevailed and killed the pro-life amendment that would have maintained existing law preventing taxpayer funds from being used for abortion.

The abortion industry does not need a government bailout! I cannot think of a greater, more important fight than to keep taxpayer funds away from the abortion industry. I can’t even imagine how many more children will be killed each year if we allow our tax-dollars to be used to end innocent lives.

We are not powerless in this fight. We can choose to have our dollars used to protect life, not end it. So I hope I can count on your support today.

For Life!  Vivat Jesu!