Why Afrezza Doesn't Need Precise Titration

[cm5]

Advanced Glycation End Products="Small Vessel Disease"=Microangioapthy =Damaged Vascular Endothelium=ED=on and on and on and on----and on----

Role of advanced glycation end products (AGEs) and receptor for AGEs (RAGE) in vascular damage in diabetes.

xp Gerontol. 2011 Apr;46(4):217-24. doi: 10.1016/j.exger.2010.11.007. Epub 2010 Nov 25.
Role of advanced glycation end products (AGEs) and receptor for AGEs (RAGE) in vascular damage in diabetes.
Yamagishi S1.
1Department of Pathophysiology and Therapeutics of Diabetic Vascular Complications, Kurume University School of Medicine, Kurume, Japan.
[e-mail]

A non-enzymatic reaction between ketones or aldehydes and the amino groups of proteins, lipids and nucleic acids contributes to the aging of macromolecules and to the development and progression of various age-related disorders such as vascular complications of diabetes, Alzheimer's disease, cancer growth and metastasis, insulin resistance and degenerative bone disease. Under hyperglycemic and/or oxidative stress conditions, this process begins with the conversion of reversible Schiff base adducts, and then to more stable, covalently-bound Amadori rearrangement products. Over a course of days to weeks, these early glycation products undergo further reactions and rearrangements to become irreversibly crossed-linked, fluorescent protein derivatives termed advanced glycation end products (AGEs). There is a growing body of evidence that AGE and their receptor RAGE (receptor for AGEs) interaction elicits oxidative stress, inflammatory reactions and thrombosis, thereby being involved in vascular aging and damage. These observations suggest that the AGE-RAGE system is a novel therapeutic target for preventing diabetic vascular complications. In this paper, we review the pathophysiological role of the AGE-RAGE-oxidative stress system and its therapeutic intervention in vascular damage in diabetes. We also discuss here the potential utility of the restriction of food-derived AGEs in diabetic vascular complications.

Small Vessel Disease of the Brain Is an Expression of a Systemic Failure in Arteriolar Function: A Unifying Hypothesis

Charlie S. Thompson, PhD; Antoine M. Hakim, OC, MD, PhD, FRCPC
From the Division of Neurology, University of Ottawa, Neuroscience Research, The Ottawa Health Research Institute, the Canadian Stroke Network, and The Heart & Stroke Foundation Centre for Stroke Recovery, Ottawa, Ontario, Canada.
Correspondence to Antoine M. Hakim, OC, MD, PhD, FRCPC, Professor & Chair, Division of Neurology, University of Ottawa, Director, Neuroscience Research, The Ottawa Health Research Institute, CEO & Scientific Director, Canadian Stroke Network, Co-Director, The Heart & Stroke Foundation Centre for Stroke Recovery, 2413-451 Smyth Road, Ottawa, Ontario K1H 8M5, Canada. E-mail [e-mail]

It is our premise that the pathophysiology of small vessel disease in the brain is similar to small vessel disease in other heavily perfused tissues and that the presence of small vessel disease elsewhere in the body foretells its presence in the brain as well as its consequences on cognitive function. The hypothesis presented in this article is that small vessel disease is a systemic condition of aging that is exacerbated by vascular risk factors, which results from dysfunction of arteriolar perfusion. This condition, which we term systemic arteriolar dysfunction, affects the brain as well as a number of extracranial systems.

Summary of Review— Recent literature is synthesized to suggest a possible etiology of this condition, highlighting the multiple pathways that may conspire to produce the endothelial and other vascular changes seen in systemic arteriolar dysfunction.

Conclusions— Regardless of the etiology, we emphasize that small vessel disease is a systemic condition with major healthcare consequences, requiring a new paradigm in the way we practice medicine. Because this condition can be decelerated by control of vascular risk factors, doing so may significantly reduce morbidity, mortality, and healthcare costs.

[mydogskip]

May 20, 2016 18:32:23 GMT -5 peppy said:

May 20, 2016 12:53:17 GMT -5 peppy said:

Blood vessel repair? Less leaking?

They do feel better on Afrezza. 

Better Nitric oxide supply and or transfer? Less cGMP degradation?

I do not think it is psychology.

Viagra stops the enzyme that PDE5, I think.

True. Excess glucose levels in the blood that is not being pulled by cells for energy and normal cell function will disrupt NO production and thus lead to ED.

Here's a very important point (no pun intended) that I need to make and would greatly boost Afrezza sales. Mannkind should do a study showing how Afrezza usage helps alleviate ED in men with Diabetes. If there is any study that could literally light a fire under the drug to get docs and especially diabetics screaming for it, it would be a study showing how Afrezza can not only stabilize BGL but help men with ED get their mojo back. Imagine looking at that Afrezza action chart that shows how quickly Afrezza acts. Now think about that same chart being paraded around but showing how quickly a guy gets sprung on Afrezza vs other drugs. Instant success like we have never seen.  And let's not ignore that NO also plays a role in female libido too. This isn't a one gender issue as the physiology of female arousement is not all that much different than males. Sex sells and if Mannkind were able to link  "Affrezza = Better Sex for Diabetics", we'd see everyone on Wall Street singing Mannkind's praise. Unfortunately, we will not see that.

[cm5]

More on Endothelial (cells lining vasculature) and NO (Nitric Oxide):

Vascular Dysfunction Associated with Type 2 Diabetes and Alzheimer’s Disease: A Potential Etiological Linkage

Med Sci Monit Basic Res. 2014; 20: 118–129.
Published online 2014 Aug 1. doi: 10.12659/MSMBR.891278
Fuzhou Wang,1,2,A,B,D,E,F,G Xirong Guo,3,B,D,E,F Xiaofeng Shen,1,B,D,E,F Richard M. Kream,4,D,E,F,G Kirk J. Mantione,4,D,E,F,G and George B. Stefano4,

Causal Relationship Between Vascular Dysfunction and Type 2 Diabetes

It is ascertained, at least in part, that a correlation exists between vascular dysfunction and the occurrence of T2DM, but we still do not know the precise causal relationship between them. Indeed, the pathology may be initiated metabolic dysregulation, leading to poor energy production in the microenvironment. Thus, the association may have existed in the beginning of the disorder and in Alzheimer’s disease (AD) as well.

Vascular dysfunction, including microvascular and macrovascular, results from DM affecting several organs (muscle, skin, heart, brain, eyes, and kidneys, et al.) [3]. The common etiology link for the different types of diabetes-associated vascular diseases is the chronic hyperglycemia that evokes pathologic responses in the vasculature, which finally cause constitutive nitric oxide (cNO) inhibition, smooth muscle cell dysfunction, overproduction of vascular endothelial growth factor (VEGF), chronic inflammation, hemodynamic dysregulation, impaired fibrinolytic ability, and enhanced platelet aggregation.

In these situations, diabetes, specifically T2DM, was considered as the initiating factor for the series of vascular diseases with the contribution of common risk factors like hypertension, tobacco use, and obesity.

In considering the consequences of these findings in DM, a negligible basal level and a diminished capacity for stimulated endothelial NO release, some of the possible potentially pathologic resultant alterations in cellular metabolism should be mentioned. Firstly, NO has been shown to have antioxidant actions [59–62]. This scavenging property gives NO a major intracellular and extracellular action against oxidative stress [61,63–70]. Emerging evidence attested the role of endothelial NO in diabetic vascular pathologies. First, endogenous NO suppresses vascular inflammation, via inhibition of p47(phox) expression, leading to attenuation of NADPH oxidase-dependent superoxide production [71]. However, selective endothelial insulin resistance itself is sufficient to induce a reduction in NO bioavailability and endothelial dysfunction that is secondary to increased generation of reactive oxygen species [72]. Third, diabetes produces a cascade of events involving production of reactive oxygen species from the NADPH oxidase leading to oxidation of BH4 and uncoupling of NOS, which promotes the oxidative inactivation of NO with subsequent formation of peroxynitrite [73]. As thus, in the absence of NO, reactive chemical species may occur and cause tissue damage [7].

[peppy]

May 21, 2016 8:16:27 GMT -5 mydogskip said:

May 20, 2016 18:32:23 GMT -5 peppy said:

Better Nitric oxide supply and or transfer? Less cGMP degradation?

I do not think it is psychology.

Viagra stops the enzyme that PDE5, I think.

True. Excess glucose levels in the blood that is not being pulled by cells for energy and normal cell function will disrupt NO production and thus lead to ED.

Here's a very important point (no pun intended) that I need to make and would greatly boost Afrezza sales. Mannkind should do a study showing how Afrezza usage helps alleviate ED in men with Diabetes. If there is any study that could literally light a fire under the drug to get docs and especially diabetics screaming for it, it would be a study showing how Afrezza can not only stabilize BGL but help men with ED get their mojo back. Imagine looking at that Afrezza action chart that shows how quickly Afrezza acts. Now think about that same chart being paraded around but showing how quickly a guy gets sprung on Afrezza vs other drugs. Instant success like we have never seen.  And let's not ignore that NO also plays a role in female libido too. This isn't a one gender issue as the physiology of female arousement is not all that much different than males. Sex sells and if Mannkind were able to link  "Affrezza = Better Sex for Diabetics", we'd see everyone on Wall Street singing Mannkind's praise. Unfortunately, we will not see that.

My ridiculously idiotic ego takes some pride in coming up with Nitric oxide as a possible reason.

Hahahaha.

[elvis2]

Thanks, I reached out to him.

[elvis2]

May 19, 2016 0:49:17 GMT -5 capnbob said:

May 18, 2016 12:58:57 GMT -5 elvis2 said:

Hello, I am new here. I found this topic after calling Mankind regarding my long tail problem with Afrezza. I started using Afrezza in January of this year, alongside my insulin pump. I definitely had to be careful, I experienced the long-tail effect while using my insulin pump for corrections and Afrezza for meals.

In April of this year, I stopped using my insulin pump and switched to 100% Afrezza with Triseba (long acting insulin). Finally A1C is coming down! But, I have noticed that I get the long-tail effect with Afrezza as well, like I did with my insulin pump (without Afrezza) when doing several corrections throughout the day. I have experienced this long tail problem ever since becoming a type 1 diabetic.

My questions to you all, when you say that titration or the long tail is less with Afrezza, does that mean I should never crash? And how long should the titration last? For example, just today I experienced a 5 hour long tail effect. I have attached a photo of this so you all can see it. when I woke up my blood sugar was in the mid-fifties.

This is not the first time I've seen this while using Afrezza, it happens often to me. But, the crash is not nearly as bad when using regular insulin.

Thoughts?

About the picture. No food, since 7pm the night before. I did miss my Triseba inject, did that at 2am. No food or drink until 9:10am.

Here is the link to my numbers showing the longtail.

drive.google.com/file/d/0B7BIGc5lm1jQMndFVjd1ZUhaNnVSVFVCdHhpbHBxem42eE53/view

You leave out too many essential details. In your google drive image, what was the nature of the last meal -- carbs, fat, protein? Are you confirming the CGM with fingersticks? What is your basal dose? What was your old lispro dose?  Why did you wait so long to deal with the hyperglycemia? Why did you take the additional dose at 4am when it appeared as though you right in the middle of the correction?  These are all things you should write down every day in detail and discuss with your diabetic nurse and/or endo.

Hi capnbob,

Let me see if I can answer all your questions:

1. what was the nature of the last meal -- carbs, fat, protein?
   I ate a low fat and carb meal. I didn't eat much to be honest.
   
   
2. Are you confirming the CGM with fingersticks?
   Yes, at least once a day, the most I will do is 4 but 1.3 a day is my average.
   
   
3. What is your basal dose?
   I use 24 units of Triseba nightly. Interestingly, I missed my basal inject the night before. Also, when I injected I had blood. Normally I don't pull out with blood. I know the instructions say not to hit a vain, don't think I did but I thought it was interesting that I had blood. I use the Novofine plus needles.
   
   
4. What was your old lispro dose?
   I was on the pump previously, my basal was 19 units a day and my total average insulin intake was 45 units a day. Weekends I used more, around 55 units.
   
   
5. Why did you wait so long to deal with the hyperglycemia?
   To be honest, I was tired and fell asleep.
   
   
6. Why did you take the additional dose at 4am when it appeared as though you right in the middle of the correction?
   After one hour, I correct, with Afrezza. I was told that after 1 hour the insulin has been used up or is no longer in the body.
   With lispro I would correct after two hours, because I knew I had to be at 180 after 2 hours with lispro.
   
   
7. I write down my daily Triseba use and make notes of anything strange or out of the norm. I use the dexcom clarity heavily to monitor my progress and send reports to my endo as needed. She also has access to my data on the clarity dexcom site.

My main question is still unanswered. Supposedly you do not crash with Afrezza, yet I can get in the 40's and 50's quite easily. 

[Deleted]

May 21, 2016 10:21:21 GMT -5 elvis2 said:

May 19, 2016 0:49:17 GMT -5 capnbob said:

You leave out too many essential details. In your google drive image, what was the nature of the last meal -- carbs, fat, protein? Are you confirming the CGM with fingersticks? What is your basal dose? What was your old lispro dose?  Why did you wait so long to deal with the hyperglycemia? Why did you take the additional dose at 4am when it appeared as though you right in the middle of the correction?  These are all things you should write down every day in detail and discuss with your diabetic nurse and/or endo.

Hi capnbob,

Let me see if I can answer all your questions:

1. what was the nature of the last meal -- carbs, fat, protein?
   I ate a low fat and carb meal. I didn't eat much to be honest.
   
   
2. Are you confirming the CGM with fingersticks?
   Yes, at least once a day, the most I will do is 4 but 1.3 a day is my average.
   
   
3. What is your basal dose?
   I use 24 units of Triseba nightly. Interestingly, I missed my basal inject the night before. Also, when I injected I had blood. Normally I don't pull out with blood. I know the instructions say not to hit a vain, don't think I did but I thought it was interesting that I had blood. I use the Novofine plus needles.
   
   
4. What was your old lispro dose?
   I was on the pump previously, my basal was 19 units a day and my total average insulin intake was 45 units a day. Weekends I used more, around 55 units.
   
   
5. Why did you wait so long to deal with the hyperglycemia?
   To be honest, I was tired and fell asleep.
   
   
6. Why did you take the additional dose at 4am when it appeared as though you right in the middle of the correction?
   After one hour, I correct, with Afrezza. I was told that after 1 hour the insulin has been used up or is no longer in the body.
   With lispro I would correct after two hours, because I knew I had to be at 180 after 2 hours with lispro.
   
   
7. I write down my daily Triseba use and make notes of anything strange or out of the norm. I use the dexcom clarity heavily to monitor my progress and send reports to my endo as needed. She also has access to my data on the clarity dexcom site.

My main question is still unanswered. Supposedly you do not crash with Afrezza, yet I can get in the 40's and 50's quite easily. 

Read Matt comments on Afrezza timing afrezzadownunder.com
You correct with Afrezza only for meals that take longer to digest so first dose after 10 min into meal and a correction dose of your sugars are still high and rising after 1 hr

[Deleted]

May 21, 2016 10:21:21 GMT -5 elvis2 said:

May 19, 2016 0:49:17 GMT -5 capnbob said:

My main question is still unanswered. Supposedly you do not crash with Afrezza, yet I can get in the 40's and 50's quite easily. 

You do not crash with afrezza cos of its short tail.. and it doesnt stay in the body like injectables ( which stay on 4 to 5 hrs )

afrezzauser.com/testing-the-limits-of-afrezza-unbelievable/

[elvis2]

Thank you peppy for the links!

[avichen]

Wow... grassroots are doing great. Anyone heard of any Afrezza hate blogs around? Other than financial analyst who hate bash the company, i'm looking for patients who hate bash Afrezza.

[sweedee79]

May 21, 2016 10:52:06 GMT -5 @iam2sekc4u2002 said:

May 21, 2016 10:21:21 GMT -5 elvis2 said:

Hi capnbob,

Let me see if I can answer all your questions:

1. what was the nature of the last meal -- carbs, fat, protein?
   I ate a low fat and carb meal. I didn't eat much to be honest.
   
   
2. Are you confirming the CGM with fingersticks?
   Yes, at least once a day, the most I will do is 4 but 1.3 a day is my average.
   
   
3. What is your basal dose?
   I use 24 units of Triseba nightly. Interestingly, I missed my basal inject the night before. Also, when I injected I had blood. Normally I don't pull out with blood. I know the instructions say not to hit a vain, don't think I did but I thought it was interesting that I had blood. I use the Novofine plus needles.
   
   
4. What was your old lispro dose?
   I was on the pump previously, my basal was 19 units a day and my total average insulin intake was 45 units a day. Weekends I used more, around 55 units.
   
   
5. Why did you wait so long to deal with the hyperglycemia?
   To be honest, I was tired and fell asleep.
   
   
6. Why did you take the additional dose at 4am when it appeared as though you right in the middle of the correction?
   After one hour, I correct, with Afrezza. I was told that after 1 hour the insulin has been used up or is no longer in the body.
   With lispro I would correct after two hours, because I knew I had to be at 180 after 2 hours with lispro.
   
   
7. I write down my daily Triseba use and make notes of anything strange or out of the norm. I use the dexcom clarity heavily to monitor my progress and send reports to my endo as needed. She also has access to my data on the clarity dexcom site.

My main question is still unanswered. Supposedly you do not crash with Afrezza, yet I can get in the 40's and 50's quite easily. 

Read Matt comments on Afrezza timing afrezzadownunder.com
You correct with Afrezza only for meals that take longer to digest so first dose after 10 min into meal and a correction dose of your sugars are still high and rising after 1 hr

I have never heard that you CANT crash on Afrezza....   its just not as easy to crash and usually it will begin to correct more rapidly because the insulin leaves faster... 

[cm5]

Hmmmm-----Sunday Brunch-----Consider AGE's  (Advanced Glycation End Products)

 www.ncbi.nlm.nih.gov/pmc/articles/PMC3704564/

Bacon, fried 5 min                                11,905
Bacon, microwaved                                1,173
Turkey, burger                                       7,426
Tofu, sautéed                                        3,212
Salmon, smoked                                      515
Egg, fried, one large                              1,237
Egg, omelet, pan, low, olive oil                  101
Bagel, toasted                                          50
Rice Krispies                                           600
Waffle, frozen, toasted                              861
Bar,Granola, peanut butter & choc chunk   953
Cantaloupe                                               20
Onion                                                      36
Tomato                                                    23
Yogurt, vanilla                                            8
Coffee, drip method                                    4
Big Mac                                               7,801

[capnbob]

May 21, 2016 10:21:21 GMT -5 elvis2 said:

May 19, 2016 0:49:17 GMT -5 capnbob said:

You leave out too many essential details. In your google drive image, what was the nature of the last meal -- carbs, fat, protein? Are you confirming the CGM with fingersticks? What is your basal dose? What was your old lispro dose?  Why did you wait so long to deal with the hyperglycemia? Why did you take the additional dose at 4am when it appeared as though you right in the middle of the correction?  These are all things you should write down every day in detail and discuss with your diabetic nurse and/or endo.

Hi capnbob,

Let me see if I can answer all your questions:

1. what was the nature of the last meal -- carbs, fat, protein?
   I ate a low fat and carb meal. I didn't eat much to be honest.
   
   
2. Are you confirming the CGM with fingersticks?
   Yes, at least once a day, the most I will do is 4 but 1.3 a day is my average.
   
   
3. What is your basal dose?
   I use 24 units of Triseba nightly. Interestingly, I missed my basal inject the night before. Also, when I injected I had blood. Normally I don't pull out with blood. I know the instructions say not to hit a vain, don't think I did but I thought it was interesting that I had blood. I use the Novofine plus needles.
   
   
4. What was your old lispro dose?
   I was on the pump previously, my basal was 19 units a day and my total average insulin intake was 45 units a day. Weekends I used more, around 55 units.
   
   
5. Why did you wait so long to deal with the hyperglycemia?
   To be honest, I was tired and fell asleep.
   
   
6. Why did you take the additional dose at 4am when it appeared as though you right in the middle of the correction?
   After one hour, I correct, with Afrezza. I was told that after 1 hour the insulin has been used up or is no longer in the body.
   With lispro I would correct after two hours, because I knew I had to be at 180 after 2 hours with lispro.
   
   
7. I write down my daily Triseba use and make notes of anything strange or out of the norm. I use the dexcom clarity heavily to monitor my progress and send reports to my endo as needed. She also has access to my data on the clarity dexcom site.

My main question is still unanswered. Supposedly you do not crash with Afrezza, yet I can get in the 40's and 50's quite easily. 

Okay, that's a little bit better. First, with regard to the fingersticks, technically you should calibrate the device twice a day to insure accuracy. Confirming during highs is mainly to insure that the device isn't broken and misleading you to overdose the insulin. For the rest of the questions, you become an endo's nightmare:

"I ate a low fat and carb meal. I didn't eat much to be honest." You need to be able to document both how much you ate as well as the proportions of the consituents including slow carbs. We not only don't know how many calories entered your system, we have no way of assaying how they were absorbed. That you spiked to high even on an assumed small meal would suggest you're "brittle" -- although you previous dosing with the pump doesn't quite suggest that. 

"Also, when I injected I had blood." Once again, you noted the blood and understood what that could mean and WHAT do the instructions say: "Never inject Tresiba® into a vein or muscle." But what did you do but go back to sleep! Under different circumstances it could have been a real long sleep. Not only that, but you tacked on an additional12U of afrezza at about the same time! When did you switch to tresiba? Your dose appears just a tad on the high side. 

"After one hour, I correct, with Afrezza." Under normal circumstances that would likely be acceptable. However this is obviously not normal circumstances and you need to examine the situation. Yes, your glucose was very high, but you gave yourself a substantial dose of tresiba -- possibly into a vein -- plus a substantial dose of afrezza to boot. The CGM clearly shows the glucose is in the process of correcting. Since you have no idea how far it's going to go you should have observed it closely to see some indication of it leveling off before any further afrezza dosing. There's no need to "jump the gun." After all, a single blood glucose of 220 isn't going to kill you but sliding down into 40-50 range is taking more serious risk. Technically, you should have waited at least an hour to see what effect the possible intravenous tresiba might be having. If that didn't show anything, then you probably should have started with a smaller dose -- perhaps even 4u -- given this particular set of circumstances. 

As regards "supposedly you do not crash with Afrezza," you always must bear in mind that everyone is different. Take a look at the PK graph on page 15 of the insert. Do you see the grey lines extending above and below each data point. Those represent the variability of absorption around that data point. Note that they are very wide with an average around 55 microunits and a range from 40 to about 70. Now look at the PD graph -- that shows the actual impact on blood glucose -- which presents an image that shows only the average effect on glucose in a group of individuals. Since each individual varies in terms of sensitivity, if you happen to get hit with 70 microunits on a particluar inhalation and you also happen to possess a high sensitivity to insulin, then depending on your meal, you could easily reach hypoglycemic levels. The main thing is to document as much as possible and then discuss it with your endo.

[agedhippie]

May 22, 2016 13:55:30 GMT -5 capnbob said:

May 21, 2016 10:21:21 GMT -5 elvis2 said:

"Also, when I injected I had blood." Once again, you noted the blood and understood what that could mean and WHAT do the instructions say: "Never inject Tresiba® into a vein or muscle."

Just to clear something up - it's almost impossible to hit a vein accidentally (as in I know of no case where it has happened) if you are injecting where you should. On the other hand from time to time you will hit a capillary.

[peppy]

May 21, 2016 8:16:27 GMT -5 mydogskip said:

May 20, 2016 18:32:23 GMT -5 peppy said:

Better Nitric oxide supply and or transfer? Less cGMP degradation?

I do not think it is psychology.

Viagra stops the enzyme that PDE5, I think.

True. Excess glucose levels in the blood that is not being pulled by cells for energy and normal cell function will disrupt NO production and thus lead to ED.

Here's a very important point (no pun intended) that I need to make and would greatly boost Afrezza sales. Mannkind should do a study showing how Afrezza usage helps alleviate ED in men with Diabetes. If there is any study that could literally light a fire under the drug to get docs and especially diabetics screaming for it, it would be a study showing how Afrezza can not only stabilize BGL but help men with ED get their mojo back. Imagine looking at that Afrezza action chart that shows how quickly Afrezza acts. Now think about that same chart being paraded around but showing how quickly a guy gets sprung on Afrezza vs other drugs. Instant success like we have never seen.  And let's not ignore that NO also plays a role in female libido too. This isn't a one gender issue as the physiology of female arousement is not all that much different than males. Sex sells and if Mannkind were able to link  "Affrezza = Better Sex for Diabetics", we'd see everyone on Wall Street singing Mannkind's praise. Unfortunately, we will not see that.

I am so el bad.

Get your sunlight men. this is the time of year for nitric oxide production.

screencast.com/t/P5dux1jY05

get it to come out of your skin

screencast.com/t/sbyvObqBqt

screencast.com/t/vLHLugh2

screencast.com/t/FvQ5FlCYnA

you can kick me off the board now

www.youtube.com/watch?v=oAAlMYWtF_s