SAFE mortgage licensing act

Mortgage Licensing Act (SAFE Act) of the Housing and Economic Recovery Act of 2008 was signed into law on July 30, 2008 to enhance consumer protection and reduce fraud in mortgage loan transactions. It requires all 50 states and 5 territories to put into place a system for licensing mortgage loan originators that meets the minimum requirements of the SAFE Act. The Conference of State Bank

Malocclusion: Disease of Civilization

In his epic work Nutrition and Physical Degeneration, Dr. Weston Price documented the abnormal dental development and susceptibility to tooth decay that accompanied the adoption of modern foods in a number of different cultures throughout the world. Although he quantified changes in cavity prevalence (sometimes finding increases as large as 1,000-fold), all we have are Price's anecdotes describing the crooked teeth, narrow arches and "dished" faces these cultures developed as they modernized.

Price published the first edition of his book in 1939. Fortunately, Nutrition and Physical Degeneration wasn't the last word on the matter. Anthropologists and archaeologists have been extending Price's findings throughout the 20th century. My favorite is Dr. Robert S. Corruccini, currently a professor of anthropology at Southern Illinois University. He published a landmark paper in 1984 titled "An Epidemiologic Transition in Dental Occlusion in World Populations" that will be our starting point for a discussion of how diet and lifestyle factors affect the development of the teeth, skull and jaw (Am J. Orthod. 86(5):419)*.

First, some background. The word occlusion refers to the manner in which the top and bottom sets of teeth come together, determined in part by the alignment between the upper jaw (maxilla) and lower jaw (mandible). There are three general categories:

• Class I occlusion: considered "ideal". The bottom incisors (front teeth) fit just behind the top incisors.
• Class II occlusion: "overbite." The bottom incisors are too far behind the top incisors. The mandible may appear small.
  
• Class III occlusion: "underbite." The bottom incisors are beyond the top incisors. The mandible protrudes.
  

Malocclusion means the teeth do not come together in a way that's considered ideal. The term "class I malocclusion" is sometimes used to describe crowded incisors when the jaws are aligning properly.

Over the course of the next several posts, I'll give an overview of the extensive literature showing that hunter-gatherers past and present have excellent occlusion, subsistence agriculturalists generally have good occlusion, and the adoption of modern foodways directly causes the crooked teeth, narrow arches and/or crowded third molars (wisdom teeth) that affect the majority of people in industrialized nations. I believe this process also affects the development of the rest of the skull, including the face and sinuses.

In his 1984 paper, Dr. Corruccini reviewed data from a number of cultures whose occlusion has been studied in detail. Most of these cultures were observed by Dr. Corruccini personally. He compared two sets of cultures: those that adhere to a traditional style of life and those that have adopted industrial foodways. For several of the cultures he studied, he compared it to another that was genetically similar. For example, the older generation of Pima indians vs. the younger generation, and rural vs. urban Punjabis. He also included data from archaeological sites and nonhuman primates. Wild animals, including nonhuman primates, almost invariably show perfect occlusion.

The last graph in the paper is the most telling. He compiled all the occlusion data into a single number called the "treatment priority index" (TPI). This is a number that represents the overall need for orthodontic treatment. A TPI of 4 or greater indicates malocclusion (the cutoff point is subjective and depends somewhat on aesthetic considerations). Here's the graph: Every single urban/industrial culture has an average TPI of greater than 4, while all the non-industrial or less industrial cultures have an average TPI below 4. This means that in industrial cultures, the average person requires orthodontic treatment to achieve good occlusion, whereas most people in more traditionally-living cultures naturally have good occlusion.

The best occlusion was in the New Britain sample, a precontact Melanesian hunter-gatherer group studied from archaeological remains. The next best occlusion was in the Libben and Dickson groups, who were early Native American agriculturalists. The Pima represent the older generation of Native Americans that was raised on a somewhat traditional agricultural diet, vs. the younger generation raised on processed reservation foods. The Chinese samples are immigrants and their descendants in Liverpool. The Punjabis represent urban vs. rural youths in Northern India. The Kentucky samples represent a traditionally-living Appalachian community, older generation vs. processed food-eating offspring. The "early black" and "black youths" samples represent older and younger generations of African-Americans in the Cleveland and St. Louis area. The "white parents/youths" sample represents different generations of American Caucasians.

The point is clear: there's something about industrialization that causes malocclusion. It's not genetic; it's a result of changes in diet and/or lifestyle. A "disease of civilization". I use that phrase loosely, because malocclusion isn't really a disease, and some cultures that qualify as civilizations retain traditional foodways and relatively good teeth. Nevertheless, it's a time-honored phrase that encompasses the wide array of health problems that occur when humans stray too far from their ecological niche. I'm going to let Dr. Corruccini wrap this post up for me:

I assert that these results serve to modify two widespread generalizations: that imperfect occlusion is not necessarily abnormal, and that prevalence of malocclusion is genetically controlled so that preventive therapy in the strict sense is not possible. Cross-cultural data dispel the notion that considerable occlusal variation [malocclusion] is inevitable or normal. Rather, it is an aberrancy of modern urbanized populations. Furthermore, the transition from predominantly good to predominantly bad occlusion repeatedly occurs within one or two generations' time in these (and other) populations, weakening arguments that explain high malocclusion prevalence genetically.

* This paper is worth reading if you get the chance. It should have been a seminal paper in the field of preventive orthodontics, which could have largely replaced conventional orthodontics by now. Dr. Corruccini is the clearest thinker on this subject I've encountered so far.

Real Estate Licensing Examinations

The Michigan real estate examinations are administered by PSI Services, LLC (PSI). The Real Estate Broker and Salesperson Candidate Information Bulletins (CIB) have been posted to PSI's website at www.psiexams.com . Follow the prompts to select "Michigan" as the state and the type of exam. The CIB details examination registration procedures and exam content.Effective December 1, 2007, prior to

Diabetics on a Low-carbohydrate Diet, Part II

I just found another very interesting study performed in Japan by Dr. Hajime Haimoto and colleagues (free full text). They took severe diabetics with an HbA1c of 10.9% and put them on a low-carbohydrate diet:

The main principle of the CRD [carbohydrate-restricted diet] was to eliminate carbohydrate-rich food twice a day at breakfast and dinner, or eliminate it three times a day at breakfast, lunch and dinner... There were no other restrictions. Patients on the CRD were permitted to eat as much protein and fat as they wanted, including saturated fat.

What happened to their blood lipids after eating all that fat for 6 months, and increasing their saturated fat intake to that of the average American? LDL decreased and HDL increased, both statistically significant. Oops. But that's water under the bridge. What we really care about here is glucose control. The patients' HbA1c (glycated hemoglobin; a measure of average blood glucose over the past several weeks) declined from 10.9 to 7.4%.

Here's a graph showing the improvement in HbA1c. Each line represents one individual:

Every single patient improved, except the "dropout" who stopped following the diet advice after 3 months (the one line that shoots back up at 6 months). And now, an inspirational anecdote from the paper:

One female patient had an increased physical activity level during the study period in spite of our instructions. However, her increase in physical activity was no more than one hour of walking per day, four days a week. She had implemented an 11% carbohydrate diet without any antidiabetic drug, and her HbA1c level decreased from 14.4% at baseline to 6.1% after 3 months and had been maintained at 5.5% after 6 months.

That patient began with the highest HbA1c and ended with the lowest. Complete glucose control using only diet and exercise. It may not work for everyone, but it's effective in some cases. The study's conclusion:

...the 30%-carbohydrate diet over 6 months led to a remarkable reduction in HbA1c levels, even among outpatients with severe type 2 diabetes, without any insulin therapy, hospital care or increase in sulfonylureas. The effectiveness of the diet may be comparable to that of insulin therapy.

Diabetics on a Low-carbohydrate Diet
The Tokelau Island Migrant Study: Diabetes

Insurance doesn't cover cancer pills!

Today, this New York Times article entitled: Insurance Lags as Cancer Care comes in a Pill revealed the communication gap between patients, doctors, technology and insurance companies.

With oral cancer drugs, “the technology has outstripped the ability of society to integrate it into the mainstream in a smooth fashion,” said Carlton Sedberry, a pharmacy expert at Medical Marketing Economics, a consulting firm.

Cancer pills provide a convenient alternative to IV chemotherapy since it reduces the number of visits that patients need to make to the hospital. However, most insurance companies do not cover these pills even though alternative therapies are covered. This makes the cost of this treatment weigh heavily in the pockets of the patients. Additionally, there may be problems with controlling dosage quantities and interpreting side effects. This new wave of cancer therapy still has a long way to go before becoming mainstream as doctors, patients and society learn to deal with the challenges that arise.

Another Fatty Liver Reversal, Part II

A month ago, I wrote about a reader "Steve" who reversed his fatty liver using a change in diet. Non-alcoholic fatty liver disease (NAFLD) is a truly disturbing modern epidemic, rare a few decades ago and now affecting roughly a quarter of the adult population of modern industrialized nations. Researchers cause NAFLD readily in rodents by feeding them industrial vegetable oils or large amounts of sugar.

Steve recently e-mailed me to update me on his condition. He also passed along his liver test results, which I've graphed below. ALT is a liver enzyme that enters the bloodstream following liver damage such as hepatitis or NAFLD. It's below 50 units/L in a healthy person*. AST is another liver enzyme that's below 35 units/L in a healthy person*.

Steve began his new diet in November of 2008 and saw a remarkable and sustained improvement in his ALT and AST levels:

Here's how Steve described his diet change to me:

I totally eliminated sugar, heavy starches, and grains. Started eating more whole, real foods, including things like grass-fed beef and pastured pork and eggs, began supplementing with good fats and omega-3 (pastured butter, coconut oil, cod liver oil). Ate more fruits and vegetables instead of refined carbs. Also completely gave up on the idea that I had to eat only "lean" meats. After my last results, the GI doc said that I wouldn't need the biopsy at all, that things were great, and that if I kept it up I "would live forever."

He did experience some side effects from this diet though:

My triglycerides also went from pre-diet measures of 201 and 147 to post diet 86, 81, and 71.

The added bonus, of course, was that my weight went from 205 pounds to 162 pounds and my body fat percentage from 24% to 12% in the matter of five months--all without the typically excessive cardio I used to try unsuccessfully for weight loss.

The liver is the body's "metabolic grand central station". It's essential for nutrient homeostasis, insulin sensitivity, detoxification, and hormone conversion, among other things. What's bad for the liver is bad for the rest of the body as well. Don't poison your liver with sugar and industrial vegetable oils.


* The cutoff depends on who you ask, but these numbers are commonly used.

How to Fatten Your Liver
Excess Omega-6 Fat Damages Infants' Livers
Health is Multi-Factorial
Fatty Liver Reversal
Another Fatty Liver Reversal

Homeless Assistance Programs

Introduction HUD's Homeless Assistance Web Page is available to help you learn more about HUD's homeless assistance programs, and to keep you informed about available funding. HUD's homeless assistance programs are broken down into two main categories, formula (non-competitive), and competitive. Competitive programs are under the umbrella of Continuum of Care. Competitive Programs

NEW LICENSING REQUIREMENTS EFFECTIVE

In February 2004, The Appraiser Qualifications Board (AQB) of the Appraisal Foundation adopted changes to the real property appraiser qualifications criteria that will become effective January 1, 2008. The requirements individuals must meet in order to become a licensed or certified appraiser will change significantly. The changes include increased requirements for qualifying education and

Real Estate Brokers and Sales Agents Licensure

Licensure. In every State and the District of Columbia, real estate brokers and sales agents must be licensed. Prospective brokers and agents must pass a written examination. The examination—more comprehensive for brokers than for agents—includes questions on basic real estate transactions and laws affecting the sale of property. Most States require candidates for the general sales license to

Like-Kind Exchanges - Real Estate Tax Tips

Generally, if you exchange business or investment property solely for business or investment property of a like-kind, no gain or loss is recognized under Internal Revenue Code Section 1031. If, as part of the exchange, you also receive other (not like-kind) property or money, gain is recognized to the extent of the other property and money received, but a loss is not recognized. Section 1031

Competing Models of Real Estate Brokerage

Traditionally, real estate brokers have performed virtually all services related to buying and selling a home, including: Marketing the home. Marketing services include listing the property in the local multiple listing service (MLS), placing advertisements in local media and on the Internet, and hosting open houses. Reviewing contracts. Contract review might include providing

Lung diseases

Lung disease is one of the top diseases in the United States today. Lung disease is on the rise worldwide. Factors such as air quality play a vital role in the increase in lung disease. Living with lung disease can be tremendously difficult, affecting daily life and the ability to do normal daily activities.

Symptoms of lung disease can vary, depending on the lung disease which has been contracted. Most lung diseases cause difficulty breathing, coughing, airway constriction, and a heavy or tight feeling in the chest. Some lung disease symptoms include fevers, weakness,heart rhythm problems or palpitations, or even blue tinting of the extremities.

Lung diseases such as lung cancers have various causative factors including, cigarette smoking, environmental or occupational exposures, and can be developed after a different type of cancer has been discovered elsewhere in the body. Asthma has hereditary factors, can be caused by second hand smoke or allergies, or other environmental factors. COPD, or chronic obstructive pulmonary disease, is usually caused by smoking cigarettes, although the chronic inhalation of marijuana can cause lung cancer and COPD. Lung diseases such as tuberculosis and legionnaires disease are caused by an infection and can be treated with very aggressive antibiotics.



There are various risk factors for lung disease, most of which are environmental, although heredity does play a role in some lung diseases such as asthma. Environmental factors include smoking or exposure to second hand smoke, exposure to toxic substances such as asbestos or chemical treatments for fiberglass, allergies, bacteria, or viruses. For instance, asthma can be triggered by second hand smoke, smoking, or allergies but can also have hereditary risk factors. Asbestos exposure creates a serious risk factor for Mesothelioma, a rare but fatal lung cancer.

Diagnosing lung disease requires a physical examination and may require tests which include chest x-rays, blood tests, and lung function tests. Asthma may be diagnosed after a physical examination, listening to the lungs of the patient to detect any wheezing, and a spirometry test which is nothing more complicated than measuring the rate of air flow expelled from the lungs. Diagnosing lung cancer is typically done with x-rays of the chest and blood tests. Phlegm may be tested for cancerous cells, a bronchoscopy or a needle biopsy may be performed, and most doctors will perform a CT scan to take detailed pictures of the inside of the lung.

Complications from lung disease can be widespread, including heart problems related from a lack of oxygen in the bloodstream. Numbness in cold weather and tingling of the extremities can also happen due to a lack of oxygen in the bloodstream. Lung disease can deteriorate the quality of life for the patient, and may eventually lead to death. While it is very rare, fatal asthma attacks have been known to occur. Lung cancer may lead to death if the cancer either can not be controlled or spreads throughout the body.

Treatment for lung disease varies by the type of disease. Asthma suffers typically use an inhaler which delivers medication straight into the bronchioles and opens the airway. Oral medication is now proving to be effective in dealing with asthma. Infectious lung diseases such as tuberculosis and legionnaires disease require high dose antibiotics. Lung cancer is often treated with either radiation treatments, chemotherapy, surgical procedures, or a combination of all three. Lung disease is a serious health risk that costs billions of dollars per year to treat, and researchers are searching for better and more effective treatments for lung disease regularly.



It is important that individuals with lung disease provide ample self care. Avoiding behaviors which are known to irritate the condition is just practical. People with lung disease should never smoke, avoid second hand smoke, avoid situations that are likely to pass germs from human to human contact or large crowded indoor areas that are likely to carry air born germs, and allergens which may affect the ability to breathe.

Coping with lung disease can be difficult and may affect every factor of daily life. Creating a comfortable sleeping environment, whether that means the use of a fan, dehumidifier, or vaporizer, is vital. Taking the appropriate medications when prescribed is also vital, whether or not the patient is symptomatic at the moment. Listening to the physician’s advice regarding diet and exercise can make a tremendous difference in the life of a lung disease sufferer.

Fair Lending

Discrimination in mortgage lending is prohibited by the federal Fair Housing Act and HUD's Office of Fair Housing and Equal Opportunity actively enforces those provisions of the law. The Fair Housing Act makes it unlawful to engage in the following practices based on race, color, national origin, religion, sex, familial status or handicap (disability): * Refuse to make a mortgage loan *

Diabetics on a Low-carbohydrate Diet

Diabetes is a disorder of glucose intolerance. What happens when a diabetic eats a low-carbohydrate diet? Here's a graph of blood glucose over a 24 hour period, in type II diabetics on their usual diet (blue and grey triangles), and after 5 weeks on a 55% carbohydrate (yellow circles) or 20% carbohydrate (blue circles) diet:


The study in question describes these volunteers as having "mild, untreated diabetes." If 270 mg/dL of blood glucose is mild diabetes, I'd hate to see severe diabetes! In any case, the low-carbohydrate, high-fat diet brought blood glucose down to an acceptable level without requiring medication.

It's interesting to note in the graph above that fasting blood glucose (18-24 hours) also fell dramatically. This probably reflects improved insulin sensitivity in the liver. The liver pumps glucose into the bloodstream when it's necessary, and insulin suppresses this. When the liver is insulin resistant, it doesn't respond to the normal signal that there's already sufficient glucose, so it releases more and increases fasting blood glucose. When other tissues are insulin resistant, they don't take up the extra glucose, also contributing to the problem.

Glycated hemoglobin (HbA1c), a measure of average blood glucose concentration over the preceding few weeks, also reflected a profound improvement in blood glucose levels in the low-carbohydrate group:

At 5 weeks, the low-carbohydrate group was still improving and headed toward normal HbA1c, while the high-carbohydrate group remained at a dangerously high level. Total cholesterol, LDL and HDL remained unchanged in both groups, while triglycerides fell dramatically in the low-carbohydrate group.

When glucose is poison, it's better to eat fat.

Graph #1 was reproduced from Volek et al. (2005), which re-plotted data from Gannon et al. (2004). Graph #2 was drawn directly from Gannon et al.

Tips for Avoiding Foreclosure

Are you having trouble keeping up with your mortgage payments? Have you received a notice from your lender asking you to contact them? Don't ignore the letters from your lender Contact your lender immediately Contact a HUD-approved Housing Counseling Agency Toll FREE (800) 569-4287 TTY (800) 877-8339 If you are unable to make

Dubai Real Estate Corporation

Dubai Real Estate Corporation (DREC) was established by His Highness Sheikh Mohammed Bin Rashid Al Maktoum, Vice-President and Prime Minister of the UAE and Ruler of Dubai, in June 2007 through Law Number 14. DREC’s activities encompass owning and managing its land bank which includes a sizable amount of properties registered under the name of the Dubai Government,as well as others

Property Management

Property Management represents wasl’s core business activity. It covers a full range of property leasing, facilities management and call centre operations and services.wasl’s leasing services include the letting of residential apartments and villas, as well as commercial units such as offices and retail outlets. We also provide staff accommodation, light industrial and warehousing units within

Paleolithic Diet Clinical Trials Part IV

Dr. Staffan Lindeberg has published a new study using the "paleolithic diet" to treat type II diabetics (free full text). Type II diabetes, formerly known as late-onset diabetes until it began appearing in children, is typically thought to develop as a result of insulin resistance (a lowered tissue response to the glucose-clearing function of insulin). This is often followed by a decrease in insulin secretion due to degeneration of the insulin-secreting pancreatic beta cells.

After Dr. Lindeberg's wild success treating patients with type II diabetes or glucose intolerance, in which he normalized the glucose tolerance of all 14 of his volunteers in 12 weeks, he set out to replicate the experiment. This time, he began with 13 men and women who had been diagnosed with type II diabetes for an average of 9 years.

Patients were put on two different diets for 3 months each. The first was a "conventional diabetes diet". I read a previous draft of the paper in which I believe they stated it was based on American Diabetes Association guidelines, but I can't find that statement in the final draft. In any case, here are the guidelines from the methods section:

The information on the Diabetes diet stated that it should aim at evenly distributed meals with increased intake of vegetables, root vegetables, dietary fiber, whole-grain bread and other whole-grain cereal products, fruits and berries, and decreased intake of total fat with more unsaturated fat. The majority of dietary energy should come from carbohydrates from foods naturally rich in carbohydrate and dietary fiber. The concepts of glycemic index and varied meals through meal planning by the Plate Model were explained [18]. Salt intake was recommended to be kept below 6 g per day.

The investigators gave the paleolithic group the following advice:

The information on the Paleolithic diet stated that it should be based on lean meat, fish, fruit, leafy and cruciferous vegetables, root vegetables, eggs and nuts, while excluding dairy products, cereal grains, beans, refined fats, sugar, candy, soft drinks, beer and extra addition of salt. The following items were recommended in limited amounts for the Paleolithic diet: eggs (≤2 per day), nuts (preferentially walnuts), dried fruit, potatoes (≤1 medium-sized per day), rapeseed or olive oil (≤1 tablespoon per day), wine (≤1 glass per day). The intake of other foods was not restricted and no advice was given with regard to proportions of food categories (e.g. animal versus plant foods). The evolutionary rationale for a Paleolithic diet and potential benefits were explained.

Neither diet was restricted in calories. After comparing the effects of the two diets for 3 months, the investigators concluded that the paleolithic diet:

• Reduced HbA1c more than the diabetes diet (a measure of average blood glucose)
• Reduced weight, BMI and waist circumference more than the diabetes diet
• Lowered blood pressure more than the diabetes diet
  
• Reduced triglycerides more than the diabetes diet
• Increased HDL more than the diabetes diet

However, the paleolithic diet was not a cure-all. At the end of the trial, 8 out of 13 patents still had diabetic blood glucose after an oral glucose tolerance test (OGTT). This is compared to 9 out of 13 for the diabetes diet. Still, 5 out of 13 with "normal" OGTT after the paleolithic diet isn't bad. The paleolithic diet also significantly reduced insulin resistance and increased glucose tolerance, although it didn't do so more than the diabetes diet.

As has been reported in other studies, paleolithic dieters ate fewer total calories than the comparison group. This is part of the reason why I believe that something in the modern diet causes hyperphagia, or excessive eating. According to the paleolithic diet studies, this food or combination of foods is neolithic, and probably resides in grains, refined sugar and/or dairy. I have my money on wheat and sugar, with a probable long-term contribution from industrial vegetable oils as well.

Were the improvements on the paleolithic diet simply due to calorie restriction? Maybe, but keep in mind that neither group was told to restrict its caloric intake. The reduction in caloric intake occurred naturally, despite the participants presumably eating to fullness. I suspect that the paleolithic diet reset the dieters' body fat set-point, after which fat began pouring out of their fat tissue. They were supplementing their diets with body fat-- 13 pounds (6 kg) of it over 3 months.

The other notable difference between the two diets, besides food types, was carbohydrate intake. The diabetes diet group ate 56% more carbohydrate than the paleo diet group, with 42% of their calories coming from it. The paleolithic group ate 32% carbohydrate. Could this have been the reason for the better outcome of the paleolithic group? I'd be surprised if it wasn't a factor. Advising a diabetic to eat a high-carbohydrate diet is like asking someone who's allergic to bee stings to fetch you some honey from your bee hive. Diabetes is a disorder of glucose intolerance. Starch is a glucose polymer.

Although to be fair, participants on the diabetes diet did improve in a number of ways. There's something to be said for eating whole foods.

This trial was actually a bit of a disappointment for me. I was hoping for a slam dunk, similar to Lindeberg's previous study that "cured" all 14 patients of glucose intolerance in 3 months. In the current study, the paleolithic diet left 8 out of 13 patients diabetic after 3 months. What was the difference? For one thing, the patients in this study had well-established diabetes with an average duration of 9 years. As Jenny Ruhl explains in her book Blood Sugar 101, type II diabetes often progresses to beta cell loss, after which the pancreas can no longer secrete an adequate amount of insulin.

This may be the critical finding of Dr. Lindeberg's two studies: type II diabetes can be prevented when it's caught at an early stage, such as pre-diabetes, whereas prolonged diabetes may cause damage that cannot be completely reversed though diet. I think this is consistent with the experience of many diabetics who have seen an improvement but not a cure from changes in diet. Please add any relevant experiences to the comments.

Collectively, the evidence from clinical trials on the "paleolithic diet" indicate that it's a very effective treatment for modern metabolic dysfunction, including excess body fat, insulin resistance and glucose intolerance. Another way of saying this is that the modern industrial diet causes metabolic dysfunction.

Paleolithic Diet Clinical Trials
Paleolithic Diet Clinical Trials Part II
One Last Thought
Paleolithic Diet Clinical Trials Part III

WASL

wasl is an Asset Management Group owned by Dubai Real Estate Corporation (DREC), created to manage and develop its assets. It aims to grow into a globally competitive entity. wasl operates a wide spectrum of property management, project management and investment management services for DREC. Key business areas that wasl is focused on are project management , property management,

Real Estate Continuing Education Course Instruction

Application and Approval• For each course, the initial application fee is $50.00. This fee is non-refundable. The check or money order must be payable to: Ohio Division of Real Estate.• Continuing education course applications may be submitted for consideration atany time during the month.NOTE: Please be advised that, to be eligible for approval of continuing educationcredit, the application form

REBA

The Real Estate and Business Agents Supervisory Board regulates the State's real estate industry. It is the independent statutory authority established under the Real Estate and Business Agents Act 1978 to regulate people who conduct real estate transactions and certain business transactions.The Board is the licensing and supervisory authority. It issues licences and certificates of

Heart failure: Heart pumps help keep the beat

If you have heart failure, a heart pump may improve your quality of life.

When you have heart failure, your heart can't pump enough blood to meet your body's needs. Treatment is directed at the underlying cause, such as high blood pressure or coronary artery disease. Lifestyle changes and medication often help, too. If heart failure progresses, an advanced treatment such as a heart pump may be recommended.

A heart pump takes over the function of one or both of the heart's lower chambers, with the potential to improve your symptoms and quality of life. Once considered a last resort for prolonging life until a donated heart became available, heart pumps have become a possible long-term treatment for selected people with heart failure.

How does a heart pump work?

A heart pump replaces the work of one or both of the heart's lower chambers (ventricles). The pump — often about the size of a personal compact disc player — is implanted in your upper abdomen through open-heart surgery. Blood from the supported ventricle flows through the pump, into the aorta and then to the rest of your body. You'll feel the pump beat beneath your skin. The pump is connected to a battery pack worn outside your body, often in a small shoulder bag or fanny pack.

Some heart pumps are designed to support only the heart's left ventricle. These are known as left ventricular assist devices (LVADs). Other heart pumps support the right ventricle (RVAD) or both ventricles (biventricular assist devices).

A bridge to recovery

Sometimes a heart pump temporarily supports the heart as it heals from a massive heart attack, an episode of sudden heart failure or complications from open-heart surgery. In other cases, a heart pump works along with medication to improve heart function until transplantation is possible. With the help of a heart pump, your heart may even perform at normal or near-normal levels — alleviating symptoms and perhaps eliminating the need for a transplant. Occasionally it's possible to be weaned from the pump until it's no longer needed.

Or sometimes a destination

If your heart failure can't be appropriately managed with medication or special pacemakers and you're not a candidate for a heart transplant, a heart pump may offer promise as a long-term treatment. This is known as destination therapy — an option approved by the Food and Drug Administration in 2002.

When used along with medication, a heart pump doubles the one-year survival rate for people with end-stage heart failure. This remarkable benefit was first noted in a 2001 landmark study in which researchers confirmed the benefits of heart pumps compared with medication alone. A heart pump also improves the signs and symptoms of heart failure — such as breathlessness and fatigue — which can improve your quality of life.

Understand the risks

A heart pump can be a lifesaving treatment. Yet the potential risks are serious, including:

• Infection
• Blood clots
• Stroke
• Bleeding
• Device malfunction

Some complications associated with a heart pump are life-threatening.

Living with a heart pump

Whether your heart pump is a bridge to transplant or your destination, you'll need to adjust to life with the pump.

• Follow the instructions from your medical team. Specific precautions may vary depending on the specific type of pump.
• Take your medication as prescribed. Your doctor may prescribe various heart failure medications, including anticoagulants to help prevent blood clots.
• Anticipate the battery life of your pump. You may need to change the pump's batteries once or even twice a day. Store extra batteries in a cool place.
• Keep it clean and dry. To prevent infection, carefully cleanse the area where the battery wire is implanted. Make sure your battery pack and the wire connecting the pack to the pump stay dry — even when you bathe.
• Avoid magnetic resonance imaging (MRI) exams. These imaging studies use a strong magnet, which may interfere with the pump.
• Watch for mechanical problems. You'll have regular check-ins with your doctor and device technician. Report any changes in the pump's sounds or motion immediately.
• Be prepared for emergencies. Your doctor will provide a hand pump and emergency power pack in case the implanted pump fails. Make sure you and your caregivers know how to use the hand pump.

A heart pump can offer a second chance at life. Work with your doctor to make the most of it.

CONSUMER TIPS – REAL ESTATE SHORT SALES

In today’s real estate market, many Missouri home buyers and sellers are considering an optionknown as a “short sale,” which allows a buyer to pay less than what’s owed on a property. Bysome estimates, short sales accounted for as much as 10 percent of all home sales nationwide inthe past year. The Missouri Real Estate Commission is warning buyers, sellers and real estatebrokers that this process

Animal Models of Atherosclerosis: Diet-Induced Atherosclerosis

LDL likely plays a role in causing atherosclerosis, with the majority of the damage coming from the oxidized form of LDL. There are at least two ways to increase the concentration of oxidized LDL (oxLDL) in the blood: 1) increase the total concentration of LDL while keeping the proportion of oxLDL the same; 2) increase the proportion of oxLDL. Dietary fats differ in their effects on these two factors, and the net outcome is also dependent on the species eating the fat and the overall dietary context.

The omega-6 polyunsaturated fat, linoleic acid (LA; found abundantly in industrial vegetable oils), may be a factor in the susceptibility of LDL to oxidation. LDL is rich in LA regardless of diet, yet the amount of LA in LDL still depends on diet to a certain degree. Thus, on the surface, one would expect a diet high in industrial vegetable oil to promote atherosclerosis. Unfortunately, it's not that simple, because LA also lowers the amount of LDL in the blood of a number of species, including humans.

The amount of atherosclerosis produced by feeding different fats depends both on how much LDL oxidation occurs and on how the fat affects the organism's blood lipid profile. For example, if corn oil lowers LDL by 3-fold relative to lard in a rabbit model, yet increases the proportion of oxLDL by 50%, the rabbit will probably develop more atherosclerosis eating lard than eating corn oil. This is because the total concentration of oxLDL is still higher in the lard group. On the other hand, if corn oil doesn't reduce LDL at all relative to lard in a rhesus monkey, yet the proportion of oxLDL increases by 50%, the corn oil group will probably develop more atherosclerosis, all else being equal.

Then there are other factors that influence atherosclerosis independently of oxLDL, such as the fat-soluble antioxidants, micronutrients and omega-6:3 ratio of the diets. It's also important to keep in mind that atherosclerosis is only one factor that influences the risk of having a heart attack.

In the last post, I argued that feeding excessive cholesterol to herbivorous or nearly herbivorous animals elevates plasma LDL greatly. In many species, saturated fat exacerbates the increase in LDL due to dietary cholesterol overload. However, in the absence of added cholesterol, several commonly used models of atherosclerosis do not show an increase in LDL upon saturated fat feeding. This is similar to the situation in humans.

Rabbits are one of the most commonly used models of diet-induced atherosclerosis. They are very sensitive to dietary cholesterol, due to the fact that their natural adult diet contains virtually none.

I recently found a great study from 1967 titled "Relative Failure of Saturated Fat in the Diet to Produce Atherosclerosis in the Rabbit" (free full text). Investigators fed rabbits cocoa butter, coconut oil and Crisco (hydrogenated cottonseed oil) at 45% of calories. They found that neither cocoa butter nor Crisco increased the rabbits' cholesterol (they didn't measure LDL directly but it typically increases in proportion to total cholesterol in rabbits), while coconut oil caused a transient increase that disappeared by 6 months on the diet. Cocoa butter caused slight atherosclerosis in some of the animals while none was detected in the coconut oil or Crisco groups.

Next, the investigators fed the rabbits cholesterol along with the fats. 0.25% cholesterol with corn oil or Crisco caused a massive (10-fold) increase in blood cholesterol, and produced atherosclerosis. They didn't pair the saturated fats with cholesterol, but the point is still clear: feeding dietary cholesterol, not saturated fat, to an herbivorous species, is the culprit.

However, subsequent studies in rabbits have shown that saturated fats can produce atherosclerosis without added cholesterol. How can this be? It turns out that it only works in the context of a highly refined "synthetic" or "semi-synthetic" diet (ref). So the dietary context plays an important role as well.

The ability of saturated fat to produce atherosclerosis in animal models requires it to cause a large enough increase in serum LDL that it overwhelms saturated fat's natural tendency to reduce LDL oxidation (relative to LA). This process is typically helped along by feeding huge amounts of cholesterol. In the absence of a large increase in LDL, atherosclerosis does not result, all else being equal.

Several studies in primates support this concept. van Jaarsveld and colleagues showed that feeding vervet monkeys 28% of calories from palm oil (SFA-MUFA), sunflower oil (PUFA) or lard (MUFA-SFA) resulted in similar LDL concentrations in the three groups. After more than two years, the palm oil group had the least atherosclerosis and the sunflower oil and lard groups were similar. It's notable that palm oil was the most saturated fat used in this study.

In another telling study by Mott and colleagues, baboons were fed diets containing 40% of calories from a predominantly saturated fat or a predominantly polyunsaturated fat. Each group was further subdivided into two groups: one receiving a small amount of cholesterol in the feed, and one receiving a large amount. Cholesterol feeding increased LDL and atherosclerosis, while the type of fat had a modest effect on LDL and no effect on atherosclerosis both at high and low cholesterol levels. I've noticed that baboons seem to throw a wrench in the gears of the mainstream conception of blood lipid metabolism.

Rudel and colleagues fed african green monkeys and cynomolgus monkeys lard (MUFA-SFA) or safflower oil (PUFA) for 40% of calories, with or without added cholesterol. Without cholesterol, both LDL and the degree of atherosclerosis were low in both monkeys fed both types of fat. Cholesterol feeding raised LDL in both species by 2-3 fold, and caused significant atherosclerosis. Atherosclerosis was more severe in monkeys fed lard plus cholesterol than in monkeys fed safflower oil plus cholesterol, correlating with their considerably higher LDL.

In sum, the ability of a fat to contribute to atherosclerosis depends in part on its ability to increase oxLDL. One way to do this is to massively raise LDL. This can be accomplished by combining dietary cholesterol overload with saturated fat in certain susceptible species. Saturated fat, in the context of a somewhat normal diet, does not appear to raise LDL very much if at all in most species, in the long term. This includes humans.

Animal models of diet-induced atherosclerosis are useful for studying the disease, but they do not support the conclusion that humans should avoid foods containing natural amounts of cholesterol and saturated fat. "Saturated fats" such as lard, palm oil, beef tallow and coconut oil probably have little or no connection to atherosclerosis in humans, or in most species eating a somewhat natural diet.

SAFE Mortgage Licensing Act of 2008

In July, Congress passed H.R. 3221, the “Housing and Economic Recovery Act of 2008,” in response to the challenges facing the real estate market, Along with the more publicized portions of the Act that provide tax benefits for selected home purchases and authorization for a takeover of Fannie Mae and Freddie Mac, the Act also significantly alters mortgage licensee regulation in the United States.

Pituitary Adenoma

What Is It?

A pituitary adenoma is a benign tumor of the anterior pituitary gland. It is the most common pituitary tumor of the gland itself. Adenoma is a general term for a benign tumor of a secreting tissue. There is no known cause in most cases of these pituitary tumors.

The pituitary gland is a small structure that lies at the base of the brain. It works closely with the brain to aid in coordination of many aspects of endocrine (hormonal) function. It is vital to the normal functioning of metabolism and other glands such as the thyroid, adrenals, mammary, testes and ovaries and even aspects of kidney function. It is comprised of an anterior pituitary (known as the adenohypophysis) as well as a posterior pituitary (called the neurohypophysis). Pituitary adenomas always arise from the anterior part.

Pituitary adenomas vary greatly from one to the next. While many are simply a mass which grows in the pituitary, several types actually secrete pituitary hormones. Rather than secreting these hormones in a normal manner, they over secrete them so that there is an over abundance of that hormone in the body. This abnormal secretion can lead to very specific clinical syndromes related to that hormone. These syndromes are described briefly below but each have a separate page to describe them in more detail.

• Prolactinoma: A pituitary tumor which secretes the hormone prolactin.
• Growth Hormone Secreting Adenoma: A pituitary adenoma which secretes growth hormone. This can lead to the syndromes of Acromegaly andGigantism.
• Cushing's Disease: A pituitary adenoma which secretes the hormone adrenocorticotropic hormone (ACTH) which stimulates the adrenal gland to secrete cortisol.
• Nonsecreting Pituitary Adenoma (Endocrine Inactive Adenoma): A pituitary tumor which does not directly secrete any hormones.
• Pituitary tumors which secrete the other anterior pituitary hormones, thyroid stimulating hormone (TSH), leutinizing hormone (LH), and follicle stimulating hormone (FSH), are all very rare. TSH secreting tumors can lead to hyperthyroidism or over secretion of thyroid hormone from the thyroid gland. Secretion of either FSH or LH can lead to loss of normal menstrual cycles and infertility in women as well as impotence and infertility in men.

In addition to the secretion of hormones, as a pituitary adenoma grows it can cause damage to the normal pituitary gland adjacent to it so that the patient may develop pituitary insufficiency of one or more hormone. Finally, with any pituitary tumor, increased secretion of prolactin (hyperprolactinemia), a hormone important for the development of breast tissue (the mammary glands), can lead to abnormal menses in women or impotence in men.

---

What Types of Symptoms Are Typical?

Presenting symptoms of pituitary tumors vary depending on the type of the tumor and its size.

Headaches: Any pituitary tumor can present with headaches.

Visual Loss: Any pituitary tumor which is large enough can cause compression of a part of the visual system in the brain which runs just above the pituitary gland. This compression can lead to loss of normal visual function which usually presents initially with loss of peripheral vision in both eyes (called homonymous hemianopsia). Some loss of visual acuity can occur as well and very large tumors that go untreated or expand quickly can lead to complete blindness. Some of this visual loss can be reversible with treatment of the tumor in some cases.

Hyperprolactinemia: Any pituitary tumor that gets big enough can interfere with the normal secretion of the hormone called prolactin. This leads to an increase in secretion of the hormone, although it does not typically get as high as from a secreting prolactinoma. This elevated prolactin can be asymptomatic but it can also cause abnormal reproductive function including loss of normal menstrual cycles in women and impotence in men. It can also lead to breast development and secretion of a milk-like substance from both men and women.

Hormone Syndromes: If a pituitary tumor secretes a hormone, additional symptoms related to that hormone can occur. For a more thorough description of those clinical syndromes, see the pages for acromegaly,gigantism, prolactinoma, and Cushing's disease.

Rarely, a pituitary adenoma can bleed suddenly (called pituitary apoplexy), causing a sudden enlargement in its size. This often leads to acute pituitary dysfunction as well as sudden loss of vision. This is generally considered a surgical emergency and most often leads to an emergent operation to remove the tumor and blood.

---

How Is The Diagnosis Typically Made?

Patients present in various ways, depending on the type of tumor they have. However, after a neurological evaluation, a CT scan or MRI scan are usually ordered to detect the tumor. The appearance of a pituitary adenoma is generally regular enough to make the diagnosis with a good degree of accuracy just based on the MRI alone. However, some related tumors can be mistaken for a pituitary tumor. Some examples of these areRathke's cleft cyst, craniopharyngioma, meningiomas of the tuberculum sellae and diaphragma sellae.

To confirm the diagnosis, tumor tissue needs to be assessed by a pathologist in most cases.

In addition the the imaging studies described above, patients with pituitary tumors will usually undergo blood tests to assess their hormonal function. The purpose of these tests is to both look for any oversecretion of hormones associated with the tumor as well as to determine if the patient has any impaired function of normal pituitary gland function. In the case ofCushing's disease, some patients will undergo inferior petrosal sinus sampling (a special blood test done by a radiologist) to confirm and refine the diagnosis.

---

What Are Some Common Treatments?

The majority of pituitary adenomas, particularly if the patient has symptoms, are treated by surgery. In most cases this involves a procedure called the transsphenoidal approach. This approach, through the nasal passages, is the most direct route to the area of the pituitary gland and is generally better tolerated with a quicker recovery than a craniotomy (opening the skull).

In patients who have loss of some normal pituitary function, they may require hormonal replacement therapy to prevent symptoms. For example, if the patient presents with low thyroid hormone, they may require treatment with synthetic thyroid hormone.

In a few cases of tumors which secrete hormones, medical therapy to control the tumor may be attempted. The most commonly used example of this is using drugs called dopamine agonists (bromocriptine and cabergoline are the most commonly used examples) in patients with prolactinoma. In some cases, this hormone will inhibit the tumor and can even cause the tumor to shrink on its own, preventing or delaying the need for surgery.

Each tumor and patient is different, so it is hard and inappropriate to make generalizations about what treatment plan is most appropriate. Each patient should discuss their options with their own physician team.

Home Inspections

Perhaps one of the most important protections a buyer and a seller can have in a home sale or purchase is a whole-house home inspection. In addition, you should have a termite or other wood-destroying insect inspection and any other type of inspection that your particular property may require.Many buyers want to save a little money by waiving their right to a home inspection. The Commission

Animal Models of Atherosclerosis: LDL

Researchers have developed a number of animal models of atherosclerosis (fatty/fibrous lesions in the arteries that influence heart attack risk) to study the factors that affect its development. In the next two posts, I will argue that these models rely on a massive increase in LDL, up to 10-fold, due to overloading the cholesterol metabolism of herbivorous species with excessive dietary cholesterol. This also greatly increases oxidized LDL, leading to atherosclerosis. I will discuss the role of saturated fat, which often receives the blame, in this process.

A reader recently sent me a reference to an interesting paper titled "Dietary Fat Saturation Effects on Low-density-lipoprotein Concentrations and Metabolism in Various Animal Models". It's a review of animal studies that have looked at the effect of different fats on LDL concentration as of 1997. They nail their colors to the mast in the first sentence of the abstract:

Saturated vegetable oils (coconut, palm, and palm kernel oil) and fats (butter and lard) are hypercholesterolemic [raise cholesterol] relative to monounsaturated and polyunsaturated vegetable oils.

But don't let this fool you; the actual data they present are much more interesting. First of all, they expressly exclude studies on models that have an "abnormal degree of response to a hypercholesterolemic diet". In other words, they attempt to create a self-fulfilling prophecy by excluding models that don't support their hypothesis. Even after stacking the deck, the data they present still fail to support their position.

When an investigator wants to study diet-induced atherosclerosis, first he selects a species that's susceptible to it. These are generally herbivorous or nearly herbivorous species such as rabbits, guinea pigs, hamsters, and several species of monkey. Then, he feeds it an "atherogenic diet". This is typically a combination of 0.1 to 1% cholesterol by weight, plus 20-40% of calories as fat. The fat can come from a variety of sources, but animal fats or saturated vegetable fats are typical. The remainder of the diet is processed grains, vitamin and mineral supplements, and often casein for protein.

Let's put that amount of cholesterol into human context. Assuming the average person eats about 2 pounds dry weight of food per day, 0.5% cholesterol would be 4.5 grams. That's the equivalent of:

• 17.5 pounds of beef steak, or
• 3.8 pounds of beef liver, or
• 22.5 eggs

Per day. Now feed that to an herbivore that's not adapted to clearing cholesterol. You can imagine it doesn't do their blood lipids any favors. For example, in one study, compared to a low-fat, low-cholesterol "control diet", a diet of 20% hydrogenated coconut oil plus 0.12% cholesterol caused hamsters' LDL to increase by more than 7-fold. A polyunsaturated fat (PUFA) rich diet caused LDL to increase less. This study is typical, and the interpretation is typical as well: SFA raises LDL. But there's another possibility that makes far more sense when you stand back and look at the data as a whole: in the absence of unnatural amounts of dietary cholesterol, PUFA reduces LDL in some species, and SFA has very little effect on it in most.

It's important to remember that this hamster experiment has little to do with the situation in humans. No one is claiming that reducing saturated fat and cholesterol will reduce a human's LDL by 7-fold. Long-term dietary interventions that reduce SFA and dietary cholesterol without increasing PUFA have little to no effect on LDL cholesterol, and can in fact increase LDL oxidation. Furthermore, humans are very resistant to blood cholesterol changes in response to dietary cholesterol, suggesting that we have an evolutionary history metabolizing it. Finally, as I've discussed in a previous post, saturated fat does not influence total blood cholesterol or LDL in humans in the long term, and the effects are modest even in the short term.

But let's get back to the animal models. The hypothesis the paper is attempting to support is that saturated fat raises LDL in a variety of (herbivorous) animal models. If that were true, it should be able to raise LDL even in the absence of added cholesterol. So let's consider only the studies that didn't add extra cholesterol to the diets. And if saturated fat raises LDL, it should also do it relative to monounsaturated fat (MUFA- like olive oil), rather than only in comparison to PUFA. So let's narrow the studies further to those that compared SFA-rich fats, MUFA-rich fats and PUFA-rich fats. In Fernandez et al. (1989), investigators fed guinea pigs 35% of calories from corn oil (PUFA), olive oil (MUFA) or lard (MUFA-SFA). Here's what their LDL looked like:
The same investigators published two more studies showing similar results over the next five years. The next study was published by Khosla et al. in 1992. They fed cebus and rhesus monkeys cholesterol-free diets containing 40% of calories from safflower oil (PUFA), high-oleic safflower oil (MUFA) or palm oil (SFA-MUFA). How was their LDL?
None of the differences were statistically significant. Khosla and colleagues published another study with the same result in 1993. This is hardly supportive of the idea that saturated fat raises LDL in animal models. The most you can say is that PUFA lowers LDL in some, but not all, species. There is no indication from these studies that SFA raises LDL in the absence of excessive dietary cholesterol. I didn't cherry pick studies here, I mentioned every study in the review paper that met my two criteria of no added cholesterol and a MUFA comparison group.

The bottom line is that experimental models of atherosclerosis rely on overloading herbivorous species with dietary cholesterol that they are not equipped to clear from their bodies. SFA does exacerbate the increase in LDL caused by cholesterol overload. But in the absence of excess cholesterol, it does not generally raise LDL even in species ill-equipped to digest these types of fats. Dietary cholesterol has little or no influence on LDL in humans. So there is no cholesterol overload for saturated fat to exacerbate. Consistent with this, saturated fat does not influence LDL in humans in the long term. This is contrary to the mainstream consensus, but is an inevitable conclusion if you carefully consider the evidence from controlled trials and observational studies.

PUFA vegetable oils do lower LDL in humans, and the effect appears to persist for at least a few years. But this is a Pyrrhic victory, as omega-6 PUFA increase LDL oxidation and exacerbate chronic inflammatory processes. Vegetable oils are not a solution to the coronary heart disease epidemic, to the contrary.

Tenancy DataBase

What is a tenancy database? Tenancy databases generally store personal information about individuals relating to defaults or alleged defaults on tenancy agreements, including failures to pay rent or damage to property. This information is usually supplied to tenancy database operators by real estate agents. The information in these databases is then accessed by real estate agents assessing

Fraud Alert