Statins increase the risk of liver damage

This study was published in the Medical Journal of Basrah University Vol: 25, No: 1 2007

Study title and authors:
Comparative Effects of Lovastatin and Simvastatin on Liver Function tests in Hyperlipidaemic Patients
Zena Sattam, Hamad Al-Jubori, Isam Hamo Mahmood
This study can be accessed at: http://www.iasj.net/iasj?func=fulltext&aId=48121

Drug-induced liver damage has become an important public health problem, contributing to more than 50% of acute liver failure cases, and there have been observations of a large number of liver failure cases on statin therapy. 

In liver function tests, liver damage is confirmed with increased levels of bilirubin and the liver enzymes; Alanine transaminase, aspartate aminotransferase and alkaline phosphatase.

This study measured the effects of statins on liver function tests. The study included: 

(i) 53 patients, aged 35-60 years, took simvastatin therapy. The simvastatin dose ranged from 10 to 20mg a day. Duration of treatment ranged from one month to four years. (Simvastatin group).
(ii) 42 patients, aged 38-60, took lovastatin therapy. The lovastatin dose ranged from 10 to 20mg a day. Duration of treatment ranged from one month to three years. (Lovastatin group).
(iii) A control group of 50 subjects, aged 35-58 who did not take statins. (No-statin group).

The study found:
(a) The alanine transaminase levels of the lovastatin group were 113% higher than the no-statin group.
(b) The aspartate aminotransferase levels of the lovastatin group were 90% higher than the no-statin group.
(c) The alkaline phosphatase levels of the lovastatin group were 11% higher than the no-statin group.(d) The bilirubin levels of the lovastatin group were 40% higher than the no-statin group.
(e) The alanine transaminase levels of the high dose (20 mg a day) lovastatin group were 181% higher than the no-statin group.
(f) The aspartate aminotransferase levels of the high dose (20 mg a day) lovastatin group were 151% higher than the no-statin group.
(g) The alkaline phosphatase levels of the high dose (20 mg a day) lovastatin group were 20% higher than the no-statin group.
(h) The bilirubin levels of the high dose (20 mg a day) lovastatin group were 72% higher than the no-statin group.
(i) The alanine transaminase levels of the long term usage (over 12 months) lovastatin group were 333% higher than the no-statin group.
(j) The aspartate aminotransferase levels of the long term usage (over 12 months) lovastatin group were 321% higher than the no-statin group.
(k) The alkaline phosphatase levels of the long term usage (over 12 months) lovastatin group were 24% higher than the no-statin group.
(l) The bilirubin levels of the long term usage (over 12 months) lovastatin group were 145% higher than the no-statin group.
(m) The alanine transaminase levels of the simvastatin group were 103% higher than the no-statin group.
(n) The aspartate aminotransferase levels of the simvastatin group were 60% higher than the no-statin group.
(o) The alkaline phosphatase levels of the simvastatin group were 6% higher than the no-statin group.(p) The bilirubin levels of the simvastatin group were 45% higher than the no-statin group.
(q) The alanine transaminase levels of the high dose (20 mg a day) simvastatin group were 150% higher than the no-statin group.
(r) The aspartate aminotransferase levels of the high dose (20 mg a day) simvastatin group were 102% higher than the no-statin group.
(s) The alkaline phosphatase levels of the high dose (20 mg a day) simvastatin group were 3% higher than the no-statin group.
(t) The bilirubin levels of the high dose (20 mg a day) simvastatin group were 55% higher than the no-statin group.
(u) The alanine transaminase levels of the long term usage (over 12 months) simvastatin group were 255% higher than the no-statin group.
(v) The aspartate aminotransferase levels of the long term usage (over 12 months) simvastatin group were 240% higher than the no-statin group.
(w) The alkaline phosphatase levels of the long term usage (over 12 months) simvastatin group were 3% higher than the no-statin group.
(x) The bilirubin levels of the long term usage (over 12 months) simvastatin group were 83% higher than the no-statin group.

The results from this study revealed significant increases of alanine transaminase, aspartate aminotransferase and bilirubin levels in the lovastatin group compared with the control group and significant increases of alanine transaminase and bilirubin in the simvastatin group when compared with the control group.

The study also revealed that the higher the dose of the statin or the longer the dose of the statin generally correlated with increased levels of the liver enzymes.

Cute Baby Chronicles: Catching up

Written on December 18, 2014...

After the initial surge of excitement which I didn't feel OK to share right away (so frustrating!) I stopped writing altogether. I'm not sure why, but I guess I was just trying to stay in the moment and experience everything as opposed to focusing on chronicling it. This post is catching us up closer to the present....

As is my habit, I've been consuming tons of information about pregnancy, child birth, and babies. I'm a bit obsessive like that. It's mostly podcasts and blogs at this stage. I just don't have the patience for books. I've listened to almost all the Pregtastic, Preggie Pals, and Birth, Baby and Life podcasts so far. So much great info!

Now, just at 20 weeks I'm starting to feel like this is really happening. I'm finally starting to show a bit (that took forever!) Careful what you wish for, I'm sure... I no longer obsessively track my food intake, but I'm working to incorporate as much good whole healthy food and I can. I've hardly gained any weight so far (and nothing in the last month before my last appointment), but I'm trying not to see that as either a good or a bad thing. My doctor isn't concerned but warned me that it WAS coming and it would be OK :) My chiefest concern is just getting the nutrition both of us really need right now.

My zeal for prenatal yoga also waned as the first trimester queasiness and fatigue set in. I haven't been to a class in awhile, but have done some at home. Now that I'm starting to feel more like myself, I plan to start attending the classes again. I really did enjoy them!

Yesterday was my latest doctor's appointment and it is so fun to listen to that heartbeat! I also got my first unsolicited "Are you pregnant question" yesterday. It was tentative, but I certainly did appreciate it! Tomorrow Cute Man and I will go for our 20 week ultrasound - the anatomy scan. Can't wait to see the little guy!

And yes, it's going to be a BOY. We already know due to a genetic test we did early on so here's to announcing the impending arrival of Samuel H. Dodson V due on or about May 5, 2015. How crazy would it be if he actually came on that date? Baby Sammy Five born on 5/5/15. Wow :) But, he'll come when he's ready (no elective inductions for me!)

Food Reward Friday

This week's lucky winner... Cheesecake Factory carrot cake!!

Read more »

Special tips to prevent cancer

Excercise to prevent cancer. Image: wallpoper.com

Although everyone has been trying to implement a healthy lifestyle, but due to the disturbed environment due to air pollution, or other reasons, the threat of disease can sometimes come on without notice. 

In addition to heart attacks and high blood pressure, cancer is a disease that is feared because it is very deadly, and not everyone can survive or recover from cancer. But someone who has cancer does not mean always die. Because in some cases there are many patients can be cured and live longer.  

If you want to prevent cancer, the foods that contain antioxidants are believed to fight cancer. Antioxidants can be obtained from green tea, garlic, peppers, and fish. In addition, you also need to avoid harmful radiation, as is also believed to be an appropriate way to avoid cancer.

A few simple things that you can make as tips to prevent cancer can be implemented as follows:

1. Reducing Sugar Intake

Need to know that my friend, the cancer cells are in the body of each person and the cancer cells need sugar to grow. Therefore dude needs to reduce the intake of sweets and starchy like potatoes, rice, and sugar.

2. Reducing red meat consumption.

Beef is one example of a delicious red meat, but red meat may trigger bowel cancer. because red meat contains saturated fat and bad cholesterol. Consume too much red meat can also lead to other diseases such as high blood pressure, and heart disease as a result of increased fat in your blood.

3. Stopping smoking

All smokers are at risk of developing cancer, let's see if the smoke mate in the pack has been given a warning that smoking can cause impotence and cancer. This is because smoking causes most of the body is poisoned. So for the smokers can attack the cancer is not just one part of the body ie the lungs, throat and mouth.

4. Drinking Green Tea

From various studies have shown that green tea can cut cancer risk if consumed regularly. This is because green tea has antioxidants that fight cancer. If you drink green tea, make sure you do not add sugar or milk in your tea.

5. Reduce drinking alcohol

Drinking too much alcohol can increase the risk of cancer, especially for women. For women who frequently consume alcohol it will be more susceptible to breast cancer. Ok .. from now on avoid alcohol

6. Begin eating organic vegetables

Organic vegetables are very good to eat one of them is to avoid cancer. Organic vegetables do not contain pesticides that can help fight cancer. So from now on try to eat organic greens. Now you can buy rice, carrots, or fruit and other vegetables are produced organically and naturally.

7. Begin consuming more fish.

To prevent cancer, the fish is very good because they contain omega-3 fatty acids are very important role to protect against the growth of cancer cells. But do not cook the fish too mature because they contain nutrients can lead to being lost. Make sure you also buy fresh fish from the supermarket or fish market that can be trusted.

8. Reducing red meat consumption.

Beef is one example of a delicious red meat, but red meat may trigger bowel cancer. because red meat contains saturated fat and bad cholesterol. Consume too much red meat can also lead to other diseases such as high blood pressure, and heart disease as a result of increased fat in your blood.

 

                                           Healthy life style can prevent cancer. Image: healthyvore.com

                                          

9. Begin consuming more fish.

To prevent cancer, the fish is very good because they contain omega-3 fatty acids are very important role to protect against the growth of cancer cells. But do not cook the fish too mature because they contain nutrients can lead to being lost. Make sure you also buy fresh fish from the supermarket or fish market that you can trust because of the cleanliness and freshness of the fish that they sell.

10. Regular exercise

By moving and sweating can help eliminate toxins from the body. So to get a healthy sweat you must exercise regularly. Do not attempt strenuous exercise enough to walk or run on the treadmill on a regular basis is enough. 

11. Eating Garlic

Eating garlic very useful because garlic is able to fight cancer at the same time is able to increase the thickness of the body. Koreans and Chinese are known as a nation that likes to eat garlic, and many of the nation's two recipes using garlic as a seasoning. Garlic is also believed to be food to maintain stamina and physical fitness.

12.  Drinking Water

Drinking enough water can help remove toxins in the body. By drinking enough water each day then you can cleanse the body system. If you do not have a problem with kidney drink plenty of water every day, but you need to keep a proper distance when you drink water so your stomach is not bloated. Of course excessive drinking water is also not good for your kidneys and stomach.

Of course there are many other ways that you can carry out to prevent cancer, so you can have a better quality of life. Begin your search for references to maximize search engine such as Google or buy books on health, so that you can get the exact reference so that you are always healthy and happy. Positive mental attitude, smile and enjoy the humor is also a way that you have always believed to make more healthy and passionate, to live a life that is highly competitive.

Cute Baby Chronicles: Containing the Excitement

This was written on August 29, 2014...

I just can't seem to contain this excitement. All I want to do is read pregnancy blogs and listen to podcasts. I've also started mining the internet for good movies. I'm all about my beloved Knocked Up and What to do When You're Expecting, but I need some variety. Suggestions welcome! I've even started looking at maternity clothes online... Soon will come the books, but I just don't have the attention span for those yet! Gotta check Audible...

Meanwhile, mum's the word of course. It feels so weird not to share something I'm THIS excited about, you know? I'm pretty sure I'll wind up spilling the beans to the fam when I visit both sides next weekend. But maybe not. I go back and forth on this. I'm definitely not mentioning it at work for obvious reasons.

As for what I usually talk about here... I'm still tracking my food in My Fitness Pal. Surprised? No, I have not developed Pregorexia (which is a very real and sad thing). However, I know that eating well is super important, now more than ever. Having a detailed record can only be helpful down the road. I changed my settings to "maintain your weight" and it seems like such a boon to eat that much! If I start to feel restricted, I will raise it or ignore the "limit". That is not what I'm doing here -- I'm not counting calories to try and avoid weight gain. I'm sure some WILL happen. But, it does serve me (and Cute Baby) well to keep things on an even keel and not go overboard with weight gain which would make things harder on me in the long run and add stress to my body, which is working hard enough as it is!

I now have my first appointment (with sonogram!) scheduled for a few weeks from now when I'll be around 8 weeks along. It feels so weird to not go in right away, like it isn't even real at this point because an expert hasn't declared me "pregnant". Well, I guess I'll just have to dig deep for some patience.... I took photos of the positive tests and my belly has felt strange all week, like very mild cramps. It might all just be in my head, but I'm rolling with it! If nothing else, my cycle is nowhere to be seen, which is of course, reassuring (and bizarre!)

And I'm very much looking forward to my second ever prenatal yoga class tomorrow :) I'm a happy mama-to-be!

Prenatal Yoga

Still waiting before posting this... Writing on August 28, 2014.

As I mentioned in my previous post, it has been a dream of mine to someday get to go to a prenatal yoga class. It seems so silly, but I was incredibly excited to have finally earned the right to go to one of these classes. The teacher and teaching assistant were both incredibly welcoming and introduced themselves to me right away, realizing I was new to the class despite the fact that the rather large studio room had over 30 women in it. They helped me set up this little incline made out of two yoga blocks and a couple of blankets plus a bolster under the knees. Although not yet necessary for me at this early stage, later on it's not recommended for pregnant women to lay flat on their backs. Regardless, it felt nice and supportive. I enjoyed it! I was just so overwhelmed with gratitude that I even felt some tears as the class got going and I was laying there, comfy and happy where I'd always wanted to be.

The class pace was perfect -- not too fast but definitely challenging. There were a few poses that we did 1 min on/1 min off to practice breathing through discomfort. Although wall-sits are difficult, they are a far cry from labor, I am sure. But the idea is there. You can survive being uncomfortable/in pain for short periods of time, especially if you know it will be intermittent.

The last part of class had us pairing up for some tandem stretching. It was nice to chat and get to know someone else in the class, which I'm sure was why they did that. The class ended with final relaxation in the supportive Sivasana pose in which we started and I again felt the tears come. I still cannot believe this is finally happening but at the same time, I have this incredible sense of peace, knowing it is the right time - the journey to this point has been completely worth it.

Tips to prevent Hepatitis C

You can prevent hepatitis C. Get special tips now and follow the simple instructions today. 

Hepatitis C is a liver disease caused by the hepatitis C, which is found in the blood of persons who have this disease. The infection is spread by contact with the blood of an infected person.

Instructions

Step 1
Hepatitis C (HCV): Hepatitis C is a serious problem for some, but not others. Most persons who get hepatitis C carry the virus for the rest of their lives. Most of these persons have some liver damage but do not feel sick from the disease. Some persons with liver damage due to HCV may develop cirrhosis of the liver and liver failure which may take many years to develop.

Step 2
You can protect yourself from HCV by minimizing your contact with human blood. For example, don’t ever shoot drugs and don’t share toothbrushes, razors, or other personal care articles.

Step 3
HCV can be spread by sex, but this does not occur very often. If you are having sex you should always get tested just to be safe.

Step 4
Hepatitis C is NOT spread by breast feeding, sneezing, hugging, coughing, sharing utensils, food, water, and casual contact.

Step 5
If you think you have Hepatitis C, ask your doctor for a blood test. Early diagnosis will help you avoid liver disease and/or further liver damage.

Tips and Warnings
• Many people who are at risk for hepatitis C are at risk for hepatitis A and B. Check with your doctor to see if you should get hepatitis A and B vaccines.

*)By dasbootjoe, eHow Member

Chocolate & Orange Popsicles

Okay, so I know putting 'popsicles' and 'hot' in the same sentence is kind of creating an oxymoron but these are in fact hot chocolate popsicles. Because you see I used this dangerously delicious vegan hot chocolate powder from Esamée Store that they were so kind to send me a while back. The only ingredients in this mix are organic coconut sugar, vegan coconut milk powder, organic raw cacao, organic cinnamon and maltodextrin. All you have to do is mix a couple of teaspoons with a cup of boiling hot water and voilà, there's a steaming cup of vegan hot chocolate for you. Yes, I am sold.

Also, chocolate and orange is a match made in heaven and I'm all about those divine flavour combinations. And there are only 5 ingredients so NO EXCUSES. You could even enjoy it in it's semi-liquid state as a beautiful chocolate milkshake!

Hot Chocolate & Orange Popsicles

Ingredients:

150 ml or 2/3 cup full fat coconut milk

150 g frozen bananas (about 1 1/2 medium sized)

1 tbsp Honest Hot Chocolate Powder from Esamée or 1 tbsp coconut sugar

1 tbsp cocoa or cacao powder

Zest from 1 organic orange

How to:

1. Slice the bananas and put them in an airtight plastic container in the freezer and leave it there for at least 8 hours to freeze.

2. Place the frozen bananas, hot chocolate powder/coconut sugar, cocoa powder and orange zest in a food processor and blend for about one minute.

3. Pour in the coconut milk through the hole on top of the food processor, little by little. Stop to scrape down the sides if necessary.

4. Divide the 'ice cream' in six popsicle moulds and freeze overnight.

5. Enjoy!

Don Matesz: Wheat Myths & The Wheat Belly Grain Brain Challenge

The Arab Bedouins traditionally consumed the
majority of energy from whole wheat bread

A recent large meta-analysis of prospective cohort studies predominantly carried out in countries where dietary fiber is derived largely from cereal fiber, in particular wheat, found that an increment of 10 grams of dietary fiber a day was associated with a 20-34%, 9% and 11% decreased risk of death from heart disease, cancer and all-causes combined, respectively.1 Similarly, recent meta-analyses have found that whole grain intake is associated with a significantly lower risk of type II diabetes, weight gain, cardiovascular disease and colorectal cancer.2 3 This data casts significant doubt on the claims that the intake of whole-grains, including whole wheat are primary causes of these conditions and diseases.

Don Matesz, author of Powerd By Plants: Natural Selection & Human Nutrition has been releasing a series of informative videos where he challenges the claims about the modernization of wheat and it being a primary cause of multiple chronic diseases and conditions. In one notable video, Don provides strong evidence that there is actually less gluten content in modern wheat, and that the intake of gluten has decreased significantly in the United States over the last century. In another video Don describes the very high intake of wheat bread in the traditional Mediterranean diet, and how bread intake was correlated with a lower rate of mortality in the Seven Countries Study, consistent with the studies described above. He is a also doing 30 day challenge where he will be consuming one pound of whole-grain wheat products, and 2-3 serving of soy products for 30 days to see whether he develops a 'wheat belly' or a 'grain brain'. Head over to his blog or YouTube channel to view his progress, or see some of the videos below.

Wheat Belly Grain Brain Challenge D5 & 6 | Wheat vs. Meat: The Mediterranean Evidence

Wheat Belly Grain Brain Challenge D7 | Does Modern Wheat Have More Gluten?

Wheat Belly Grain Brain Challenge D9 | Is Commercial Wheat Loaded With Toxic Pesticides?

While Don is only doing a 30 day challenge, a number of healthy populations have traditionally consumed similar or even greater quantities of wheat throughout their entire lives. One example described previously are the Arab Bedouins, who traditionally consumed the great majority of their dietary intake from whole wheat bread (approx. 750 grams in addition to other wheat products).4 5 Obesity, diabetes and heart disease were all exceptionally rare in this population when they adhered to their traditional whole wheat based diet, and have become far more common since the transition towards a westernized diet.4 6 It is past time to cast aside the unsubstantiated claims made by fad diet promoters about the adverse health effects of modern wheat and whole grains.

Vegan Macaroni and Cheese

Behold my attempt to veganize this good old classic loved and cherished by people all over the world. Here in Sweden it goes by 'Makaronipudding', which literally means 'Macaroni Pudding'.  I know for you English people that's something else but this is the kind of mac 'n' cheese that most people are familiar with; the savoury one. 

But how does one make macaroni and cheese without the cheese? Well, there's this wonderful little thing called nutritional yeast that can replace the cheese. I know, cheese addicts out there, this may seem hard to grasp. Because yeast? Doesn't sound so appealing. But it is! Since going vegan, I don't think a single day has gone by without me using it in at least something. It adds a cheesy, savoury flavour that is just too good for words. Another of the reasons why I love it so much is because one single tablespoon provides you with almost all of the B-vitamins that you need. One tablespoon!

So I hope I've convinced you to start incorporating this miracle ingredient into more of your meals. And vegans, this is especially directed at you. Buy it. Just do it.

Vegan Macaroni and Cheese

Serves: 1

3 oz./80 g uncooked brown rice pasta, preferably macaroni or fusilli (or pasta of your choice)

4 oz./110g silken tofu, firm

2 tbsp nutritional yeast

1 1/2 - 2 tbsp vegan cream substitute (such as Oatly iMat 15%)

1 tsp lemon juice

1 pinch nutmeg

Cherry tomatoes (optional)

Salt and pepper to taste

How to:

1. Boil pasta according to instructions on package.

2. Pre-heat oven to 200C

3. Put the remaining ingredients in a small bowl and blend with a hand blender until smooth. Season as you go, don't skimp on the salt but don't use too little either!

4. When the pasta is done, drain and pour it into the bowl with the 'cheese' sauce. Stir well and make sure that all the pasta is covered with sauce.

5. Pour the 'macaroni and cheese' into 1-2 ramekins or a small casserole like the one on the picture. Halve cherry tomatoes and put a few on top. 

6. Sprinkle with some additional nutritional yeast and bake in the oven for 25 minutes. Check it now and then to make sure it doesn't burn on top!

7. Serve immediately.

Healthy Baby On the Way!

I have just reached 20 weeks so I'm ready to start sharing my thoughts... I planned to wait until I hit the magical 12 week mark to start posting these updates. It was very hard to contain my excitement but I totally get why waiting until then is the convention. 12 weeks came and went and somehow, I still wasn't quite ready. But here, at the halfway point, it's time to let it fly! 

This post was written on August 27, 2014 -- the day after I got my positive test. I just cannot wait to start cataloging this journey! So, for now, this is just for me with the idea of posting these updates starting in a couple months.

I am still very much in shock. It's been over 4 years of not preventing conception, with only one other pregnancy, which was an extremely early miscarriage that happened before I knew I had been pregnant. It was traumatic physically, but emotionally I just couldn't process that I had lost something I didn't even know I'd had. My doctor thought it was ectopic (a tubal pregnancy) because they didn't see anything on ultrasound, despite my insistence that I could only possibly be a day or two pregnant due to knowing my cycle. They did eventually see something in the uterus, but it was not viable by that point in any case. 

That was two years ago and since then, nothing. I went through periods of actively charting my cycle and doing tons of research and planning. I also went through times when I couldn't think about it at all. I needed to enjoy my life the way it is, which is fantastic. 

All the time, the clock was ticking... I was staring at my 37th birthday and just knew that it was now or never in terms of taking a proactive approach. I saw my doctor, got some preliminary tests (all seemed fine). Sam was checked. We started jumping through the hoops my insurance needed for our referral to the fertility center (dealing with two different sets of medical systems -- Kaiser and GW was quite the fun time!) 

I signed up for a Yoga for Fertility Class. I joined Baby Launch Camp. I worked with a Health Coach. I downloaded Fertility Meditations. I recommitted to daily temperature and fertility sign charting. I was on this! But, somewhere in the back of my mind was Negative Nelly whispering how this just wasn't going to happen for us. I started looking into adoption and foster care (the latter something we want to do eventually, regardless of whether was have a biological child). Those are great options that I support but there was this niggling craving to have this all-too-human experience. I wanted to find out "for sure" (at least as much as the medical establishment can determine this) before exploring other options. 

I'm not sure what "did it" this month. Not much has really changed -- I still eat a Paleo diet, which has been including Perfect Health Diet starches to varying degrees. I had been counting calories and slowly losing a bit of weight (nothing significant yet). The main difference is that I did put my intention on the process to a much greater degree. 

I also read somewhere that stevia is used for contraception in some cultures (totally controversial and not an established fact) so I stopped using it. I had been using it quite a bit in smoothies and coffee/tea. I'm telling you, if that turns out to have been the issue I will scream! I was trying to avoid sugar at all costs only to be undermining my fertility? So wrong! But, who knows? These days, I'm working to eat things without a sweet taste and to use honey sparingly when I really want it. Sugar is sugar, but at least the body knows how to process glucose/fructose. I figure that small amounts won't cause too much trouble. The idea is to avoid the dreaded blood sugar spikes. 

That brings me to several days ago when I realized that my temperatures weren't starting to drop in advance of my expected period. That was a good sign! Then, a few more days went by... And yesterday, I decided what the heck? Just take a test. And it was positive! I could not believe it. So, I took another one. Also positive! Seriously? Was this really happening? I stared at the sticks for a minute or so, then ran down two flights to find Cute Man. He was surprised but very happy! 

I contacted my doctor right away to ask to take a blood test to confirm. She said that it wasn't needed and that the home tests are accurate. I should just make an appointment in a few weeks for my first sonogram. Really? It didn't seem like it could be official without a doctor pronouncing me pregnant. Even so, I know in my heart it's true -- it's happening. I have such a wave of joy that has just permeated everything for the last two days. And tonight, I'm going to my very first prenatal yoga class! Is it weird that I've dreamed of going to prenatal yoga? It's like a club that I just couldn't get into. Now, I have my free pass  and I'm not wasting any time taking advantage of it! 

Atorvastatin linked to abnormally high calcium levels

This paper was published in the Archives of the Turkish Society of Cardiology 2014 Oct;42(7):662-6

 

Study title and authors:

Can atorvastatin calcium cause asymptomatic hypercalcemia?

Ipekçi SH, Baldane S, Sözen M, Kebapçılar L

Department of Internal Medicine, Division of Endocrinology and Metabolism, Selcuk University Faculty of Medicine, Konya, Turkey.

 

This paper can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/25490303

Hypercalcemia is a condition in which the calcium level in your blood is above normal. Too much calcium in your blood can weaken your bones, create kidney stones, and interfere with the way your heart and brain works.

This paper reports the case of a woman who developed hypercalcemia after starting atorvastatin.

(i) A 52-year-old female was referred to hospital for hypercalcemia.
(ii) She had been taking atorvastatin for 1.5 years.
(iii) Atorvastatin induced hypercalcemia was suspected.
(iii) Exhaustive tests were conducted that ruled out all other causes of hypercalcemia.
(iv) She stopped taking atorvastatin and her calcium levels returned to normal.
(v) She restarted atorvastatin and again her hypercalcemia returned.
(vi) She again stopped taking atorvastatin and her calcium levels returned to normal.

Is Meat Unhealthy? Part V

In this post, I'll examine the possible relationship between meat intake and type 2 diabetes.  Type 2 diabetes is the most common form of diabetes, and it is strongly linked to lifestyle factors.

Non-industrial cultures

Non-industrial cultures have an extremely low prevalence of diabetes, whether they are near-vegan or near-carnivorous.  This is supported by blood glucose measurements in a variety of cultures, from the sweet potato farmers of the New Guinea highlands to the arctic Inuit hunters.  Here is what Otto Schaefer, director of the Northern Medical Research Unit at Charles Camsell hospital in Edmonton, Canada, had to say about the Inuit in the excellent book Western Diseases (Trowell and Burkitt, 1981):
Read more »

Third Annual Squash Hunger Event!

The Greenhouse is collaborating with the Healthy World Cafe and the York County Food Alliance for the third annual Squash Hunger event. Squash Hunger is an event in which people come together to recover, preserve and share food in the community. Farmers from around Pennsylvania are setting aside their excess produce to be transformed into a delicious and nutritious soup for those in need. Please join us in sorting, preparing and freezing a bounty of squash soup. The soup will be donated to a host of groups working to end hunger in the York area.

The Greenhouse is a community organization dedicated to saving and sharing healthy food. We do this by recovering food that would have otherwise been wasted, preserving it in healthy and creative ways and then distributing it to the community.

You can help – We need volunteers and donations. Sign-Up at our "Volunteer Spot" link on this website.

Donations of containers, sweet potatoes, onions, garlic, carrots, cayenne, nutmeg, thyme, salt and pepper welcome.

Squash Hunger will take place on the weekend of the Martin Luther King, Jr. Day of Service.

More specifically, the event is scheduled for:
Friday January 16th 6 p.m. to 9 p.m.
Saturday January 17th from 9 a.m. to 1 p.m.
Sunday January 18th from 8 am to 12 noon and 1 p.m. to 5 p.m.
Monday January 19th from 8 am to 12 noon and 1 p.m. to 5 p.m.

Stay tuned for more details. This event is currently scheduled to take place at the Healthy World Cafe, 24 S. George Street, York, PA.

Gingerbread pancakes with a Vegan Frosting

We're continuing with the Christmas theme here on the blog and next up is this basic recipe for gingerbread pancakes with a vegan lucuma-vanilla frosting... yum! I usually make my pancakes with a mix of coconut flour and buckwheat flour but I've been suspecting for a while now that it's the coconut flour that make the pancakes go all soft and gooey inside, big no-no if you're not into eating raw batter! So I completely omitted it and these turned out perfectly moist and fluffy, just like they're supposed to be. A perfect start to any winter day.

Gingerbread pancakes with a Vegan Frosting

Pancakes:

1/2 cup (70g) buckwheat flour

1/2 tsp baking powder

1/4 tsp baking soda

1 1/2 tsp gingerbread spice mix (cinnamon, ginger, cloves)

1 chia egg (1 tbsp ground chia seeds mixed with 3 tbsp water)

1 small banana, mashed (approximately 80 g)

3-4 tbsp almond milk

1 tsp apple cider vinegar or lemon juice

How to:
1. First, prepare your vegan 'buttermilk' by mixing the almond milk with the apple cider vinegar. Set aside to curdle.
2. Now prepare your chia egg: Grind one tbsp of whole chia seeds either by hand or in a coffee grinder, then mix the ground seeds with 3 tbsp of water. Stir well and let sit on the side for a few minutes to swell.
3. In a small bowl, mix the buckwheat flour, baking powder and baking soda well until they're evenly divided. 
4. Mash the banana with a fork or blitz it a couple of times with a hand blender if you don't want any clumps whatsoever left.
3. Pour in the chia egg, mashed banana and 'buttermilk' and stir until the batter is completely smooth. Let sit on the countertop for a few minutes (the batter should be THICK)
4. Fry in a spoonful of coconut oil (unless you have a non-stick frying pan) on medium heat for a couple of minutes on each side.

Vanilla-Lucuma Frosting

4 oz/108 g silken tofu

1 tbsp lucuma powder

1 pinch vanilla powder

2 dates, pitted and (if you want) peeled

1 tsp melted coconut oil (optional)

How to:
1. Blend all ingredients with a hand blender until smooth. Place a spoonful of frosting between each pancake, save a dollop for the top and serve with fresh fruit!

Saturated Fat and Heart Disease Meta-Analyses: Were Scientists Wrong?

Was it Ancel Keys or the low carb advocates
who fabricated data on saturated fat?

In a previous review, Clearing up the Confusion Surrounding Saturated Fat, I examined several important flaws and omissions in two meta-analysis studies which are frequently cited as evidence against the hypothesis that dietary saturated fat increases the risk of heart disease. The earlier study was published in 2010 by Siri-Tarino and colleagues in the American Journal of Clinical Nutrition, and the more recent study published by Chowdhury and colleagues in the Annals of Internal Medicine. These studies were both cited in a recent Time magazine article by Bryan Walsh as evidence to "eat butter" for health. In this earlier review I focused primarily on how the studies included in these meta-analyses, as well many other studies actually provide support for the hypothesis that saturated fat increases the risk of fatal forms of heart disease.

Although a number of prominent diet-heart researchers identified many serious flaws and omissions in these meta-analyses that cast doubt on the validity of the researchers conclusions, there are several other critical flaws related to how the estimates were derived for these meta-analyses that have not received adequate attention.1 2 3 4 5 This review will examine how a number of erroneous estimates may have biased the results and primary findings of these meta-analyses. Of particular concern, is in regards to how Siri-Tarino and colleagues derived negative estimates for three studies for which the original peer reviewed publications found positive associations between saturated fat and risk of heart disease. These studies and the estimates published in the meta-analysis by Siri-Tarino and colleagues are described in the table below. 

Study Name                                Risk Ratio (RR)    95% Confidence Interval (95% CI)

Framingham Heart Study6         0.92                       0.68, 1.24

Honolulu Heart Study7               0.86                       0.67, 1.12

Lipid Research Clinics Study8    0.97                       0.80, 1.18

Note: The risk ratio represents high vs low intake of saturated fat in relation to coronary heart disease. An estimate below 1 suggests a benefit of higher intake, and vice-versa. The estimates are considered statistically significant only if both the lower and upper 95% confidence intervals are on either side of 1.

The estimates published in the meta-analysis by Siri-Tarino and colleagues for all three of the abovementioned studies suggest a non-significant trend towards a benefit of saturated fat intake, greatly contrasting the findings from the original peer reviewed publications.9 This warrants an investigation into how Siri-Tarino and colleagues derived these negative estimates.

The Framingham Heart Study

Contrary to other studies included in the meta-analysis, the Framingham study reported estimated risk ratios for low vs high intake, rather than high vs low intake of saturated fat. Among the younger cohort in this study, 10% vs 15% of intake was associated with a 22% decreased risk of coronary heart disease (RR=0.78 [95% CI, 0.61-1.00]).6 Conversely this benefit of low intake was not observed among the older cohort (RR=1.06 [95% CI, 0.86-1.30]). Nevertheless, both of these estimates were controlled for serum cholesterol, which is expected to have biased these findings against showing an adverse effect of saturated fat. 

The tables in the meta-analysis clearly show that rather than converting the risk ratios for low vs high intake to appropriately reflect high vs low intake, Siri-Tarino and colleagues simply reported the estimates for 10% vs 15% of intake as representing 15% vs 10% of intake of saturated fat. The combined estimate for the younger and older groups in this cohort should therefore have been reported as RR=1.09 [95% CI, 0.81-1.47], and not as RR=0.92 [95% CI, 0.68-1.24], which was the estimate reported in the meta-analysis. The estimate provided in the meta-analysis for this study is clearly erroneous and biased the meta-analysis against showing an adverse effect of saturated fat.

The Honolulu Heart Study

In the original peer reviewed publication from the 10 year follow-up of the Honolulu Heart Study, a high intake of saturated fat was associated with a highly statistically significant increased risk of incidence of combined myocardial infarction (heart attack) and coronary heart death.7 This was despite over-adjustment for serum cholesterol. However, when combined with the incidence of the soft end points, angina and coronary insufficiency, the association was only statistically significant in the univariate analysis which did not control for serum cholesterol. The authors of this paper however, warned about misinterpreting the results for these soft end points, asserting:

When interpreting these results about whether the nutrients relate differently to the different manifestations of coronary heart disease, one should keep several problems in mind. The diagnostic certainty of the soft end points (angina pectoris or coronary insufficiency) is much less than that of the hard end points (myocardial infarction or coronary heart disease death).This could result in attenuation of a true relationship.

In the meta-analysis by Siri-Tarino and colleagues, the estimates for the 10 year follow-up of the Honolulu Heart Study were derived not from a peer reviewed publication, but rather from a separate data set obtained from the NHLBI. The primary reason that these estimates provided in the meta-analysis greatly contrasted with that of the peer reviewed publication can likely be explained by difference in the inclusion criteria of the participants. The tables in the meta-analysis show that the data used was based on 1177 cases of coronary heart disease from 8006 participants. However, in the peer reviewed publication there was a total of only 456 cases of coronary heart disease from 7088 participants.  Due to several important factors, the researchers of the original peer reviewed publication excluded 918 of the total 8006 participants from their analysis, asserting:

Men who reported that their intake was atypical for the day covered by the 24 hour recall, or who could not recall their intake, were excluded from the present analyses (n=502). Additionally, all men assessed as being prevalent cases of coronary heart disease (n=301), stroke (n=111), or cancer (n=49) were excluded from the analyses.

It is therefore evident that more than 60% of coronary events included in the meta-analysis for this particular study occurred in participants who had pre-existing disease at study baseline and/or reported unreliable dietary intake. As these additional participants made up less than 12% of the population, yet experienced more than 60% of the total events, this suggests the likelihood that these events occurred primarily among the participants with pre-existing cardiovascular disease, rather than the healthy participants reporting unreliable dietary intake. It should be noted that Siri-Tarino and colleagues clearly stated that one of the inclusion criteria for the meta-analysis was that “study participants were generally healthy adults at study baseline”, suggesting that the data they selected did not meet their own criteria.

When considering the fact that the estimate for this study used in the meta-analysis was negatively associated with coronary heart disease, rather than positively associated as was the case in the peer reviewed publication, this suggests that the participants excluded in the peer reviewed publication who experienced coronary events, largely being those with pre-existing disease, were reporting a lower intake of saturated fat. This is concerning considering the evidence that people who are diagnosed of being at risk of cardiovascular disease tend to limit saturated fat intake post-diagnosis. For example, in the earliest study included in the meta-analysis, participants diagnosed with high cholesterol had a tendency to reduce intake of saturated fat in order to improve risk factors.10 It should therefore not be surprising that participants with established cardiovascular disease likely reported a lower intake of saturated fat in this study, suggesting that a lower reported intake was only a marker of more disease, rather than a cause of it. This phenomenon is known as reverse causality, and is one of the important reasons why participants with pre-existing disease are either excluded, or examined separately from healthy participants in such studies. The inclusion of such data in a meta-analysis could significantly distort the findings. 

It is not entirely clear why a null estimate was reported for this study in the more recent meta-analysis published by Chowdhury and colleagues. However, the sample size described in supplement section of the meta-analysis paper suggests that the estimates were based on the same misleading data used by Siri-Tarino and colleagues, and not the original peer reviewed publication.11

The Lipid Research Clinics Study

In the Lipid Research Clinics study, it was observed that among the younger cohort that a 1% increased intake of energy from saturated fat was associated was a statistically significant 11% increased risk of death from coronary heart disease (RR=1.11 [95% CI, 1.04-1.18]).8 However, similar to the Framingham study, this study also included over-adjustments for serum cholesterol and the adverse effect of a high intake of saturated fat was not apparent among the older cohort (RR=0.96 [95% CI, 0.88-1.05]).

In the meta-analysis by Siri-Tarino and colleagues, the estimate for both the younger and older cohorts combined using the random-effects model was reported as RR=0.97 [95% CI, 0.80-1.18]. It is clear that this estimate is erroneous. When using the random-effects model for two estimates, the estimate with the narrowest confidence intervals should carry more weight, and therefore the combined estimate should have been much closer to the estimate for that of the younger cohort. The estimate for a 1% increase of energy from saturated fat should have been reported as RR=1.04 [95% CI, 0.90-1.19]. Similar to the abovementioned studies, this erroneous estimate biased the meta-analysis against showing an adverse effect of saturated fat.

Reanalysis of the Data

The use of erroneous estimates for several studies included in the meta-analysis by Siri-Tarino and colleagues warrants a reanalysis of the original data. I therefore performed a revised meta-analysis of the same 16 prospective cohort studies included in this meta-analysis. The methods used to derive the estimates have been described previously, and were mostly consistent with those used by Siri-Tarino and colleagues. For the Honolulu Heart Study, I derived the estimates based on only the hard coronary end points due to the concern of the accuracy of the estimates for the soft end points being less certain. As the exact P-value was not available for this publication, and indicated only as being between 0.01 and 0.001, I chose to derive the corresponding standard error using a P-value of 0.01, as this was the most conservative estimate.7

In a meta-analysis based on the 16 studies included in the meta-analysis published by Siri-Tarino and colleagues, dietary saturated fat intake was associated with a statistically significant 16% increased risk of coronary heart disease (Fig. 1).

FIGURE 1. Risk ratios and 95% CIs for fully adjusted random-effects models examining associations between saturated fat intake in relation to incidence of coronary heart disease. ¹Studies that included adjustments for serum or LDL cholesterol. SAT, saturated fat intake.

I also carried out an updated meta-analysis, including prospective cohort studies published up until November 2014 that provided the necessary data to derive risk ratios and the corresponding 95% confidence intervals. If a study was published multiple times, the estimate for the longest period of follow-up was used. A total of 21 studies were included, including recent publications not included in either the meta-analyses by Siri-Tarino and colleagues, and Chowdhury and colleagues.7 8 9 12 13 14 15 16 17 18 19 20 21 22 23 24 25 In a meta-analysis of 21 studies, dietary saturated fat was associated with a statistically significant 15% increased risk of coronary heart disease (Fig. 2).

FIGURE 2. Risk ratios and 95% CIs for fully adjusted random-effects models examining associations between saturated fat intake in relation to incidence of coronary heart disease. ¹Studies that included adjustments for serum or LDL cholesterol. SAT, saturated fat intake.

The findings from these meta-analyses presented here are compatible with the findings from a broad range of evidence described previously. This includes findings from randomized controlled trials showing an adverse effect of saturated fat on blood cholesterol and arterial function, as well as the demonstrated unequivocal causal relationship between diets rich in cholesterol and saturated fat, and the development of atherosclerosis in nonhuman primates, among dozens of other animal species. Furthermore, these findings are supported by numerous ecological studies, including the Seven Countries Study. 

The estimates of this meta-analysis are clearly stronger than that of the Siri-Tarino and Chowdhury meta-analyses, neither of which produced statistically significant estimates. One of the primary reasons for these contrasting estimates was due to the correction of the estimates for several studies described above. These contrasting estimates can also in part be explained by the correction of erroneous estimates for the confidence intervals reported in the Siri-Tarino meta-analysis for the Ireland-Boston Diet Heart Study, and in the Chowdhury meta-analysis for the EPIC-Greece study. It is clear that in the original peer reviewed publications that the estimates in these studies were statistically significant to the 95% confidence level, yet non-statistically significant estimates were reported in the meta-analyses for these studies, biasing against showing an adverse effect of saturated fat.13 20

Another important difference in the meta-analyses presented here, is that the estimates for studies reporting estimates as a 1% increase of energy were transformed to represent a 5% increase of energy from saturated fat. In the Siri-Tarino meta-analysis the researchers either simply reported the estimates for a 1% increase, or transformed the estimates to represent a similarly small increase of energy. Similarly, Chowdhury and colleagues multiplied the estimates from these studies by the power of 2.18, effectively representing the effect of an increase of only a 2.18% increase of energy. The researchers rational for this was that this equation would be expected to show the effect of mean top vs bottom third of intake. While this equation may be suitable for some studies using different scales of measurement, it requires a leap of faith to assume a difference of only 2.18% of energy represents high vs low intake in these studies. Reporting estimates as a 5% increase of energy, as was done here would make differences for high vs low intake much more comparable to that of the other included studies, while still being moderately conservative. As the studies that reported estimates as a 1% increase of energy were more likely to show a positive relationship between saturated fat and coronary heart disease, failing to transform the estimates to represent a sufficient change in intake may result in minimizing the statistical power of these studies, and in-turn biasing a meta-analysis against showing an adverse effect of saturated fat.

Conflicts of Interest

The meta-analyses published by Siri-Tarino and colleagues and Chowdhury and colleagues contained erroneous estimates for several positive studies which in-turn biased against showing an adverse effect of saturated fat. Given the fact that these researchers were well informed in this area of research, it is difficult to accept that they were simply unaware of any of the issues described here. In the meta-analysis by Siri-Tarino and colleagues there was clear evidence of potential conflicts of interest. The meta-analysis was funded in part by the National Dairy Council, and the senior researcher, Ronald Krauss had reported receiving grants from the National Dairy Council, the National Cattleman’s Beef Association and the Robert C. and Veronica Atkins Foundation. Similarly, several of the researchers of the meta-analysis by Chowdhury and colleagues have reported receiving grants from the food industry. Suggestive evidence of these researchers intention to downplay the role of saturated fat on fatal heart disease have also been described previously.

Although receiving grants from a particular industry does not necessarily negate the findings of a study, when errors are made that bias the study results in favor of the concerned industry, the intentions of the researchers should be questioned. The lines of evidence described here lends support to the likelihood that these researchers put their own interests before that of the general public, driving the public to follow dangerous dietary patterns at the hands of fad diet advocates who promote these studies.

Putting Data into Context

It is important to note that the influence that saturated fat has on the risk of disease is not primarily determined by intake per se, but by which foods saturated fat is substituted for. As the intake of dietary fiber was universally low among participants in these studies, this suggests that participants consuming diets lower in saturated fat were substituting saturated fat primarily with lean animal foods and heavily processed foods.26 In addition, as dietary fiber was associated with a decreased risk of coronary heart disease in a number of these studies, the estimates described here therefore could be a significant underestimation of the effect of replacing saturated fat with more healthful, fiber rich foods.26 Furthermore, in the studies included in this meta-analysis, the difference for high vs low intake of saturated fat was relatively low, often only ranging between about 5% and 10% of energy. This suggests that individuals following popular diets which emphasize far greater intakes of saturated fat than recommended levels may be at a much greater risk.

It is also important to note that the effect that a particular food has on the risk of coronary heart disease cannot be fully explained by the amount of one particular nutrient, but rather by multiple nutrients that likely operate together in a complex manner to modify the risk of disease. Therefore, it would be more appropriate to compare the substitution of different foods, rather than focusing entirely on substituting single nutrients. Focusing attention on recommending healthy dietary patterns that are naturally low in saturated fat, while rich in dietary fiber and other beneficial nutrients; primarily, minimally processed, plant-based diets would likely be a more effective measure to improve overall dietary quality, resulting in greater improvements to heart health compared to the more contemporary reductionist approach of focusing on modifying single nutrients. The effectiveness of such a diet was recently demonstrated again by Caldwell Esselstyn in a follow-up of 200 high-risk patients. In this study, coronary artery disease was either arrested or reversed in the great majority of adherent patients, clearly contrasting that of any other peer-reviewed study of similar size.27

This review demonstrates that the conclusions of several meta-analysis studies which suggest that dietary saturated fat unlikely increases the risk of heart disease are misleading, and that the current evidence supports the recommendations to replace foods rich in saturated fat with minimally refined plant based foods. Recommendations based on the findings of these meta-analyses made by the media and low carb advocates to consume more saturated fat rich foods are therefore unsubstantiated and likely dangerous. While it may make an interesting read being told that scientists, such as Ancel Keys have intentionally deceived us into believing that saturated fat-rich foods are unhealthy, it is appears that it may actually be the authors of such articles who lack in the way of honesty. 

Study acronyms: ATBC, Alpha-Tocopherol Beta Carotene Study; BLSA, Baltimore Longitudinal Study of Aging; EPIC-Greece, European Prospective Investigation into Cancer Greece; EUROASPIRE, European Action on Secondary and Primary Prevention through intervention to reduce events; FHS, Framingham Heart Study; GPS, Glostrup Population Study; HHS, Honolulu Heart Study; HLS, Health and Lifestyle Survey; HPFS, Health Professionals' Follow-Up Study; IBDH, Ireland-Boston Diet Heart Study; IIHD, Israeli Ischemic Heart Disease Study; JACC, Japan Collaborative Cohort Study; JPHC, Japan Public Health Center Based Study; KIHD, Kuopio Ischaemic Heart Disease Risk Factor Study; LRC, Lipid Research Clinics; MALMO, Malmo Diet and Cancer Study; NHS, Nurses' Health Study; SHS, Strong Heart Study; WES, Western Electric Study.