10 Fatloss Questions You Should Be Asking ( Part 1 )

[ Editor’s Note:  Fitness author Jon Benson shared this letter with me and gave me permission to share it with you. ]

There’s stuff you know.

Then there’s stuff you don’t know.

But the key to success in anything is the discovery of one other variable:

The things you don’t know you don’t know.

Think about that.

So many people ask me questions like…

— How can I get rid of my stubborn bodyfat?
— How fast can I do it?
— What’s the best dietplan for me?

These are good questions, don’t get me wrong.

But there are at least 10 questions most people never know to ask.

It’s the stuff they didn’t know they didn’t know… make sense?

Today we’ll cover 3 of the 10…

HIDDEN QUESTION 1:
“What’s The Best Dietary-Fat To Eat To Get Rid Of Bodyfat?”

Sounds nutty, doesn’t it?

The media loves to deceive you when it comes to dietary fats… and I’m here to set the record straight:

You absolutely must consume dietary fat in order to burn-off your bodyfat.

There’s an old saying:  “Fat burns…but in the presence of dietary-fat.”

It’s true.

There are actually two “Best Fats” you should be eating:

Coconut Oil
CLA

Coconut oil is ideal to cook with. Use that in place of all the starchy foods you may be eating. You’ll get leaner faster… and you’ll be a ton more healthy too.

Coconut oil keeps you satisfied longer, lubricates your joints, and yes… actually helps you get rid of stubborn bodyfat.

Use 1 tablespoon per 50 lbs per day, but be sure to decrease your starchy carbs (breads, rice, potatoes, etc.)

CLA is a form of (gasp!) transfat… but it’s a healthy form that helps your body get rid of bodyfat. You can only get it in supplement-form… well, that’s the best way.

I personally take 4 grams per day. Jarrow is my favorite brand. You can get it at most health food stores.

I cover several other fats you need to eat in my video and book, found here:

HIDDEN QUESTION 2:
“Why Is Cardio Bad For Me?”

Okay… that’s an over-statement. It’s not ‘bad’ for you… it’s just not nearly as ‘good’ for you as the media and magazines want you to believe.

Especially if you do it the way they suggest: Too long, too frequently.

Do it the way I suggest and watch what happens.

First, spend 80% of your exercise time doing ‘resistance’ training, not cardio… but rest very brief between sets.

My newest update to “7 Minute Muscle” is called “7 Minute Body”. It combines both “7 Minute Muscle” and an additional 100 or so pages of in-home ONLY workouts.

That way you can train in the gym… or in your home… and get it done in 7 to 14 minutes a day. Done!

You will be shaping your body and burning-off some major calories at the same time… all without boring cardio.

Then when you “do” cardio, do it the way I detail in “7 Minute Body”… use the 9-minute GXP Cardio Workout.

Add simple walking to this several days a week and your cardio is set.

GXP works because it is progressive and does not over-tax the recovery system. You warm up, then hit about 85% of your max effort, then cool down.

But the key is ‘when’ to do it… and that’s covered in my book.

I still enjoy sitting on my bike and watching TV, but I do that just to burn-off those last bits of bodyfat. Most of you do not need to do this.

It’s a waste of time for the masses… but resistance training is not.

Oh, one more thing:  Runners have a far higher degree of heart attacks than non-runners. So cardio ‘can’ be bad for you if you over-do it.

NOTE:  You can pick up “7 Minute Body” at 77% off…
but only if you get EODD…

More here:

HIDDEN QUESTION 3:
“How Does Pizza Help Me Shed Bodyfat?”

Sounds like a dream, doesn’t it?

Think again.

My dietary plan not only “lets” you eat pizza (or whatever your favorite foods might be) every week, several times a week… it DEMANDS that you do it.

What the…. ?

Yep. Here’s why.

First, I have you eat less on certain days and certain times. If done the way I suggest your metabolism (the rate you use fat, energy, etc.) will not slow down that much.

Then… at a specific time… boom!  You eat a lot more food… and the best way to do this is eating your favorite foods.

First, they usually have more calories.. duh!  Second, you’ll ENJOY the freakin’ process! Most “diets” fail because people hate them… too restrictive.

So I created my System from the ground up to ensure I never got bored with my eating… and the extra cals from pizza (or my favorite… Mexican… or Key Lime Pie… yum) actually boosts my metabolism sky-high.

Here’s an example:

Last week I ate the normal Every Other Day Diet-way… for me it’s the “Extreme Plan” (there are 4 Plans, each for different goals.)

So, after several days of lower-cal, lower-carb eating, I ate about 5000 calories of Mexican food (so good!) But the TIMING is crucial. You just can wing it. Don’t worry… I tell you exactly when to do it.

The next morning I saw more of my abs.

I went back to EODD-style eating, which I love btw… and then later had some Key Lime Pie… and what do you know? Leaner the next day.

Now I’m doing this as I “peak” — I have to be in top shape in December. The only time I stop this is 4 weeks prior to a photoshoot… but unless you want to be 5% bodyfat (and you probably do not) you never have to stop it.

Works like a charm.

Watch this and find out why:

Yours In Fitness,

J O N   B E N S O N

P.S.  Special freebie to those who watch my entire presentation on the page above… very nice… : )

Coffee May Reduce Prostate Cancer Risk

Regular coffee consumption is associated with a striking decrease in fatal or metastatic prostate cancer, according to an analysis of long-term data from the Health Professionals Follow-up Study.

Kathryn M. Wilson, ScD, with the Department of Epidemiology at the Harvard School of Public Health, Boston, Massachusetts, and colleagues led the new study, reported online May 17 in the Journal of the National Cancer Institute.

According to the researchers, coffee contains “diverse biologically active compounds that include caffeine, minerals, and phytochemicals.” They add that many studies suggest that long-term coffee drinking may be linked to improved glucose metabolism and insulin secretion.

Using data from the prospective Health Professionals Follow-up Study, the researchers analyzed information from 47,911 men who reported intake of regular and decaffeinated coffee first in 1986 and were observed every 4 years thereafter.

From 1986 to 2006, there were 5035 of the 47,911 men who had developed prostate cancer; of those, 642 patients had so-called lethal prostate cancers, defined as fatal or metastatic. The study participants overall consumed an average of 1.9 cups of coffee per day.

Among men drinking at least 6 cups per day, the adjusted risk for overall prostate cancer was 18% lower vs that in nondrinkers (relative risk [RR], 0.82; 95% confidence interval [CI], 0.68 – 0.98; P linear trend = .10).

Notably, the risk was decreased by approximately 60% in this group vs nondrinkers (RR, 0.40; 95% CI, 0.22 – 0.75; P trend = .03) when only lethal forms of prostate cancer were considered.

The researchers also found that coffee consumption did not appear to be associated with a decreased risk for nonadvanced or low-grade cancers and only slightly correlated with a reduced risk for high-grade cancer.

However, both caffeinated and decaffeinated coffee appeared to decrease the risk for lethal prostate cancer. For each cup, the risk declined by approximately 6% for regular coffee (RR, 0.94; 95% CI, 0.88 – 1.01; P = .08) and by roughly 9% for decaffeinated coffee (RR, 0.91; 95% CI, 0.83 – 1.00; P = .05).

Men drinking at least 6 cups a day had an age-adjusted incidence of only 425 prostate cancers per 100,000 person-years vs 529 in those not consuming coffee. Likewise, the incidence of lethal prostate cancers was 34 vs 79 per 100,000 person-years in those drinking at least 6 cups vs nondrinkers, respectively.

“It is premature to recommend that men increase coffee intake to reduce advanced prostate cancer risk based on this single study,” Dr. Wilson and colleagues conclude. “In addition, the effects of coffee consumption on other aspects of health must be considered in making consumption recommendations,” they add. “However, our findings are potentially important, given the lack of identified modifiable risk factors for advanced prostate cancer.”

According to the researchers, coffee may provide as much as half of total antioxidant intake in many settings. Compounds in coffee that may affect cancer risk could include chlorogenic acids, which inhibit glucose absorption; quinides, the roasting products of chlorogenic acids; and lignans, phytoestrogens with potent antioxidant activity that may benefit glucose.

~Emma Hitt, PhD

Even A Serious Health Scare May Not Be Enough To Get Patients To Improve Health Habits

In the Los Angeles Times Share to FacebookShare to Twitter (5/23) “The MD” column, Valerie Ulene, MD, a preventive medicine specialist, observes that “even a serious health scare may not be enough” to get patients to shake habits deleterious to their health, such as eating too much salt, smoking, drinking too much, or not exercising. This is the case, even though “after a serious illness, lifestyle changes often have the potential to dramatically improve a person’s overall health and quality of life. In fact, lifestyle factors such as smoking, diet and physical activity strongly influence how rapidly many diseases will progress.”

National Eye Institute Estimates Approximately 15,000 Infants Born With ROP Each Year

On its website, WTVQ-TV Lexington, KY (5/23, Runyon), an ABC affiliate, reported, “The National Eye Institute estimates about 14,000 to 16,000 infants are born with” retinopathy of prematurity (ROP) each year. “In severe cases, retinal detachment can cause significant vision impairment or blindness.” Sadly, “each year, up to 1,500 infants require medical treatment for ROP and 600 become legally blind from the condition.”

Retinopathy of prematurity

From Wikipedia, the free encyclopedia


Retinopathy of prematurity
(ROP), previously known as retrolental fibroplasia (RLF), is an eye disease that affects prematurely born babies. It is thought to be caused by disorganized growth of retinal blood vesselswhich may result in scarring and retinal detachment. ROP can be mild and may resolve spontaneously, but may lead to blindness in serious cases. As such, all preterm babies are at risk for ROP, and very low birth weight is an additional risk factor. Both oxygen toxicity and relative hypoxia can contribute to the development of ROP.


Pathophysiology

Normally, maturation of the retina proceeds in-utero, and at term the mature infant has fully vascularized retina. However, in preterm infants, the retina is often not fully vascularized. ROP occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. The key disease element is fibrovascular proliferation. This is growth of abnormal new vessels that may regress, but frequently progresses. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Multiple factors can determine whether the disease progresses, including overall health, birth weight, the stage of ROP at initial diagnosis, and the presence or absence of “plus disease”. Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of ROP, and may raise the risk of other hypoxia-related systemic complications.

Patients with ROP are at greater risk for strabismus, glaucoma, cataracts and myopia later in life, and should be examined yearly to help prevent and treat these conditions.

Diagnosis

Following pupillary dilation using eye drops, the retina is examined using a special lighted instrument (an indirect ophthalmoscope). The peripheral portions of the retina are sometimes pushed into view using scleral depression. Examination of the retina of a premature infant is performed to determine how far the retinal blood vessels have grown (the zone), and whether or not the vessels are growing flat along the wall of the eye (the stage). Once the vessels have grown into Zone 3 (see below) it is usually safe to discharge the child from further screening for ROP. The stage of ROP refers to the character of the leading edge of growing retinal blood vessels (at the vascular-avascular border). The stages of ROP disease have been defined by the International Classification of Retinopathy of Prematurity (ICROP).

Retinal examination with scleral depression is generally recommended for patients born before 30–32 weeks gestation, with birthweight 1500 grams or less, or at the discretion of the treating neonatologist. The initial examination is usually performed at 4–6 weeks of life, and then repeated every 1–3 weeks until vascularization is complete (or until disease progression mandates treatment).

In older patients the appearance of the disease is less well described but includes the residua of the ICROP stages as well as secondary retinal responses.

Differential diagnosis

The most difficult aspect of the differential diagnosis may arise from the similarity of two other diseases:

  • exudative vitreoretinopathy which is a genetic disorder that also disrupts the retinal vascularization in full-term infants.
  • Persistent Fetal Vascular Syndrome also known as Persistent Hyperplastic Primary Vitreous that can cause a traction retinal detachment difficult to differentiate but typically unilateral.

International classification of retinopathy of prematurity (ICROP)

The system used for describing the findings of active ROP is entitled The International Classification of Retinopathy of Prematurity (ICROP).[1] ICROP uses a number of parameters to describe the disease. They are location of the disease into zones (1, 2, and 3), the circumferential extent of the disease based on the clock hours (1-12), the severity of the disease (stage 1-5) and the presence or absence of “Plus Disease”. Each aspect of the classification has a technical definition. This classification was used for the major clinical trials. It has been revised in 2005[2]

 

Zones of the retina in ROP

The zones are centered on the optic nerve. Zone 1 is the posterior zone of the retina, defined as the circle with a radius extending from the optic nerve to double the distance to the macula. Zone 2 is an annulus with the inner border defined by zone 1 and the outer border defined by the radius defined as the distance from the optic nerve to the nasal ora serrata. Zone 3 is the residual temporal crescent of the retina.

The circumferential extent of the disease is described in segments as if the top of the eye were 12 on the face of a clock. For example one might report that there is stage 1 disease for 3 clock hours from 4 to 7 o’clock. (The extent is a bit less important since the treatment indications from the Early Treatment for ROP[3])

The Stages describe the ophthalmoscopic findings at the junction between the vascularized and avascular retina.

  • Stage 1 is a faint demarcation line.
  • Stage 2 is an elevated ridge.
  • Stage 3 is extraretinal fibrovascular tissue.
  • Stage 4 is sub-total retinal detachment.
  • Stage 5 is total retinal detachment.

In addition, Plus disease may be present at any stage. It describes a significant level of vascular dilation and tortuosity observed at the posterior retinal vessels. This reflects the increase of blood flow through the retina. [1]

Prognosis

Stages 1 and 2 do not lead to blindness. However, they can progress to the more severe stages. Threshold disease is defined as disease that has a 50% likelihood of progressing to retinal detachment. Threshold disease is considered to be present when stage 3 ROP is present in either zone I or zone II, with at least 5 continuous or 8 total clock hours of disease, and the presence of plus disease.[4] Progression to stage 4 (partial retinal detachment), or to stage 5 (total retinal detachment), will result in substantial or total loss of vision for the infant.

Monitoring

In order to allow timely intervention, a system of monitoring is undertaken for infants at risk of developing ROP. These monitoring protocols differ geographically because the definition of high-risk is not uniform or perfectly defined. In the USA the consensus statement of experts is informed by data derived by clinical trials and published in Pediatrics 2006. They included infants with birthweights under 1500 grams or under 30 weeks gestation in most cases.

Treatment

Diagram of an eye, in cross-section. 

The retina (red) is detached at the top of the eye.

Diagram of an eye with a scleral buckle, in cross-section. 

The silicone band (scleral buckle, blue) is placed around the eye. This brings the wall of the eye into contact with the detached retina, allowing the retina to re-attach.

  • Peripheral retinal ablation is the mainstay of ROP treatment. The destruction of the avascular retina is performed with a solid state laser photocoagulation device, as these are easily portable to the operating room orneonatal ICU. Cryotherapy, an earlier technique in which regional retinal destruction was done using a probe to freeze the desired areas, has also been evaluated in multi-center clinical trials as an effective modality for prevention and treatment of ROP. However, when laser treatment is available, cryotherapy is no longer preferred for routine avascular retinal ablation in premature babies, due to the side effects of inflammation and lid swelling.
  • Scleral buckling and/or vitrectomy surgery may be considered for severe ROP (stage 4 and 5) for eyes that progress to retinal detachment. Few centers in the world specialize in this surgery, because of its attendant surgical risks and generally poor outcomes.
  • Intravitreal injection of bevacizumab (Avastin) has been reported as a supportive measure in aggressive posterior retinopathy of prematurity.[5]

In a recent clinical trial comparing bevacizumab with conventional laser therapy, intravitreal bevacizumab monotherapy showed a significant benefit for zone I but not zone II disease when used to treat infants with stage 3+ retinopathy of prematurity. (New England Journal of Medicine 2011 364(7):603-615)

History

A significant time in the history of the disease was between 1941–1953, when a worldwide epidemic of ROP was seen. Over 12,000 babies worldwide were not only born with the disease but blinded by it. Soul musician Stevie Wonder, actor Tom Sullivan as well as jazz singer Diane Schuur are a few famous people who have the disease.

The first case of the epidemic was seen on St. Valentine’s Day in 1941, when a premature baby in Boston was diagnosed. Cases were then seen all over the world and the cause was, at that point, unknown. By 1951 a clear link between incidence and affluence became clear: many cases were seen in developed countries with organized and well-funded health care. Two British scientists suggested that it was oxygen toxicity that caused the disease. Babies born prematurely in such affluent areas were treated in incubators which had artificially high levels of oxygen. Studies on rats made this cause seem more likely, but the link was eventually confirmed by a controversial study undertaken by American pediatricians. The study involved two groups of babies. Some were given the usual oxygen concentrations in their incubators, while the other group had “curtailed” oxygen levels. The latter group was shown to have a lower incidence of the disease. As a result, oxygen levels in incubators were lowered and consequently the epidemic was halted.[6]